Pocket Guide To Nut Crd

Pocket Guide to Nutrition Assessment of the Patient with Chronic Kidney Disease 3rd Edition

Developed by the Council on Renal Nutrition of the National Kidney Foundation Editor:

Primary Reviewers: Secondary Reviewers:

Linda McCann, RD, CSR, LD Satellite Healthcare Redwood City, CA Alice Chan, RD, CSR, LD Houston, Texas Lori Lambert, MS, RD, CDE Boston, MA Susan Reams, RD, CSR, LD Des Moines, IA Nancy Spinozzi, RD (Peds) Boston, MA

FORWARD This revision of the Pocket Guide was undertaken to update trends in clinical practice and to incorporate the recommendations of the National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI). Every effort was made to obtain and provide the most up to date information. Where information differs from previous versions or references, the most recent was used. As is common with such a resource, and in view of the rapidly developing K/DOQI guidelines, it is difficult to find a point at which publication moves forward rather than wait for new guidelines and initiatives. Thus, the revision and review process has been lengthy, affecting the publication of this edition of the pocket guide. For those who are new to this resource, the primary goal has been to compile nutrition assessment information in a concise and abbreviated format so that it could truly be a “pocket guide.” In the interest of keeping it concise each piece of information is evaluated for inclusion with that primary goal in mind. The balance between too much and too little information is difficult to achieve because of the wide variation of practice within the target audience. For experienced clinicians, the book may provide a concentrated source of information they know and use on a regular basis. For the less experienced clinician, it may provide a base on which to build clinical expertise. My hope is that the Pocket Guide will provide tools that enhance the commitment to consistent, high quality nutrition care for all chronic kidney disease (CKD) patients. Where appropriate and available, references are cited for further exploration of a particular topic. The book is not all inclusive. In some cases the information is a compilation from many sources and input from experienced renal dietitians. On almost every topic there will be varied opinions. The information herein is not meant to dictate clinical practice, but to provide practical resources. It is the responsibility of individual clinicians to keep their knowledge base current and to interpret and modify their resources to reflect the policies, procedures, and philosophies of the specific practice setting. -Linda McCann, RD, CSR, LD

This book was published with an educational grant to the NKF-Council on Renal Nutrition from

Redwood City, CA www.satellitehealth.com Net Nutrition A-Z

30 East 33rd Street New York, NY 10016 (800) 889-2210 www.kidney.org

The K/DOQI seal ensures accurate interpretation of the K/DOQI clinical practice guidelines. The symbol has been added to the pages that were reviewed and approved by K/DOQI.

© 2005 National Kidney Foundation, Inc. All Rights Reserved

Pocket Guide to Nutrition Assessment of the Patient with Chronic Kidney Disease

Acronyms and Abbreviations AA/aa - Amino acids ABW – Adjusted body weight AIDS- Acquired immune deficiency syndrome ARF - Acute renal failure APD - Automated Peritoneal Dialysis( )TjETEMC /P
Pocket Guide to Nutrition Assessment of the Patient with Chronic Kidney Disease TABLE OF CONTENTS

Introduction Chapter 1: Nutrition Assessment Charts, Tables, and Formulas Practical Steps to Nutrition Assessment - Adult Patients K/DOQI Assessment and Monitoring Recommendations Tips for Effective Assessment, Interviewing, and Teaching Height Estimation From Knee Height Height Estimation From Arm Span Determination of Frame Size by Elbow Breadth Determination of Frame Size by Wrist Circumference Patient Determined Frame Size Methods to Determine Body Weights for Nutrient Calculations Standard Body Weight Metropolitan Life Height and Weight Tables for Adults-Male Metropolitan Life Height and Weight Tables for Adults-Female Weight for Height Tables for Filipinos Desirable Body Weight Based on BMI Estimating Dry Weight Clinical Signs of Fluid Status In Dialysis Patients Usual Fluid Intake and Output in Adults Without Kidney Disease Weight Comparison Formulas Adjusted Body Weight for the Obese or Underweight Patient Weight Estimation in Amputees Body Mass Index Body Mass Index Classifications Creatinine Index (For estimating Edema-free Lean Body Mass) Sample Calculation of Edema-free Lean Body Mass Body Surface Area Nomogram Body Surface Area Formulas Arm Anthropometrics Reference Values for the Triceps Skinfold Thickness – Male Reference Values for the Triceps Skinfold Thickness – Female Reference Values for Mid-arm Muscle Circumference - Male/Female Reference Values for Mid-upper Arm Muscle Area – Male Reference Values for Mid-upper Arm Muscle Area – Female Other Measures of Body Composition Subjective Global Assessment Criteria For Estimation of Performance or Functional Status Dietetic-Specific Nutritional Diagnostic Codes (D-S NDCs) Medical Nutrition Therapy (MNT) Common Physical Signs of Malnutrition © 2005 National Kidney Foundation, Inc. All Rights Reserved

1-2 1-3 1-4 1-5 1-6 1-7 1-8 1-9 1-10 1-11 1-12 1-13 1-14 1-15 1-16 1-17 1-17 1-18 1-19 1-20 1-21 1-22 1-23 1-24 1-25 1-26 1-27 1-28 1-29 1-30 1-31 1-32 1-33 1-34 to 1-41 1-42 1-43 to 1-47 1-48 1-49 to 1-50 1

Pocket Guide to Nutrition Assessment of the Patient with Chronic Kidney Disease Chapter 2: Laboratory Values/Drug Nutrient Interactions General Information Conversion Formulas Laboratory Tests Possible Non-Dietary Causes of Hyperkalemia in Kidney Disease Signs and Symptoms of Abnormal Serum Potassium Acidosis/Acidemia Acidosis/Alkalosis Na+/K+ Content of Salt and Salt Substitutes Drugs That May Impair Absorption or Utilization of Nutrients Drug Nutrient Interactions Potential Nutrition Effects of Common Immunosuppressive Drugs Herbal Supplements

2-2 2-3 2-4 to 2-18 2-19 2-20 2-21 2-22 2-23 2-24 2-25 2-26 2-27 to 2-28

Chapter 3: Nutrient Calculations General Information Daily Nutrient Recommendations for Kidney Disease Nutrition Recommendations for CKD Patients Not on Dialysis L-Carnitine Supplementation in MD Patients Nutrient Recommendations for the Pregnant Dialysis Patient Nutrient Recommendations for AIDS Harris Benedict Formula for Determining Basal Energy Expenditure Suggested Adjustment Factors for Energy Needs During Acute Illness Estimated Body Weight and Energy Needs in Para- and Quadriplegia Estimates of Calories Absorbed From Peritoneal Dialysate National Renal Diet Food Choice Lists (Nutrient Averages) Vitamins Formulated for CKD Patients Considerations for a Kosher Diet Available Fiber, Potassium, and Phosphorus in Common High Fiber Cereals Composition of Milk and Milk Substitutes Chapter 4: Special Considerations for the Diabetic Patient Common Symptoms, Treatments, and Definitions of Diabetes Stages of Diabetic Nephropathy Recommended Dietary Modification in Diabetic Nephropathy Types and Actions of Insulin Oral Hypoglycemic Agents Glycated Hemoglobin Hypoglycemia Modifications for Acute Illness in Insulin Dependent DM Food Glucose Equivalents to 15 gm Carbohydrate Diabetic Gastroparesis Other Nutrition Issues for Diabetics

© 2005 National Kidney Foundation, Inc. All Rights Reserved

3-2 3-3 to 3-4 3-5 3-6 3-7 3-8 3-9 3-9 3-10 3-11 to 3-12 3-13 to 3-14 3-15 3-16 3-17 3-18

4-2 4-3 4-4 4-5 4-6 4-7 4-8 4-9 4-10 4-11 4-12

2

Pocket Guide to Nutrition Assessment of the Patient with Chronic Kidney Disease Chapter 5: Special Considerations for the Elderly Patient Education Considerations for the Elderly DETERMINE: A Nutrition Checklist for the Elderly Potential Influences on Nutrition Status in the Elderly Physiological Changes in the Elderly Body Composition Changes in the Elderly Decrease in Physiological Function at 80 Years of Age Incidence of Malnutrition in the Elderly Subjective Global Assessment

5-2 5-3 5-4 5-5 5-6 5-6 5-7 5-8

Chapter 6: Hyperlipidemia in CKD General Patterns of Hyperlipidemia in CKD Patients At Risk for Developing Cardiovascular Complications National Cholesterol Education Program (HCEP) Target Lipid Levels/Therapeutic Lifestyle Changes Antihyperlipidemic Drugs Approximate Cholesterol Content of Common Foods

6-2 6-3 6-4 6-5 6-6 to 6-7 6-8

Chapter 7: Anemia in CKD Anemia Terminology Used to Describe Cell Alterations in Anemia Types and Characteristics of Anemia Laboratory Values Used to Diagnose Anemia Interpretation of Iron Status Parameters Iron Balance in CKD Patients Laboratory Values Used to Diagnose Iron Deficiency in CKD Estimation of Iron Needs: Recommendations for Repletion Iron Supplements Reasons for Inadequate Response to Epogen therapy

7-2 7-2 7-3 7-4 7-5 7-6 7-7 7-8 7-9 7-10

Chapter 8: Bone Metabolism and Disease in CKD/Urolithiasis Management of Osteodystrophy in CKD Osteodystrophy of CKD: Types and Characteristics Negative Effects of Hyperphosphatemia Hyperphosphatemia Due to Release of Phosphorus From Bone Phosphorus Density of Common Foods Phosphate Binding and Calcium Supplementation Calcium Compounds Potential Side Effects of Calcium-Based Binders Common Name Brands of Calcium-Based Binders/Supplements Combination Binders with Calcium Other Phosphate Binders Available Vitamin D and Vitamin D Analogs-Oral and IV Use of Active Vitamin D or Vitamin D Analogs Protocols for the Administration of Vitamin D and Vitamin D Analogs

8-2 8-3 8-4 8-4 8-5 8-6 8-7 8-7 8-8 8-8 8-9 8-10 8-11 8-12

© 2005 National Kidney Foundation, Inc. All Rights Reserved

3

Pocket Guide to Nutrition Assessment of the Patient with Chronic Kidney Disease Chapter 8: Bone Metabolism and Disease in CKD/Urolithiasis (cont) Manufacturers’ Suggested Dosing Guidelines for Vitamin D or Analogs Factors Affecting Therapeutic Response to Vitamin D/analogs in Hyperparathyroidism Management of Adynamic (Low Turnover) Bone Disease Formulas for Adjusted Calcium/Ionized Calcium Calculation Symptoms of Hyper- and Hypocalcemia Etiology of Hypercalcemia Potential Indications for Parathyroidectomy Common Clinical Course After Parathyroidectomy Urolithiasis (Nephrolithiasis/Kidney Stones) Treatment of Calcium Stones Hyperoxaluria Oxalate Content of Common Foods Soft Tissue Calcification and Calcific Uremic Arteriopathy (Calciphylaxis) Chapter 9: Malnutrition in CKD Adult Malnutrition Factors that Can Cause or Exacerbate Malnutrition in CKD Evaluation of Weight Loss Over Time Critical Proteins for Assessing Malnutrition Guidelines for Enteral Feeding Enteral Nutrition Supplements Specialty Nutrition Bars/Cookies/Puddings Modular Products Oral Amino Acids Tube Feedings-Special Considerations for CKD Common Tube Feeding Sites Tube Feeding Formulas Common Tube Feeding Products Intradialytic Parenteral Nutrition (IDPN) Gastrointestinal Motility Studies IDPN Solutions Recommended TPN Solution for Acute or CKD Nutrient Calculations for Parenteral Nutrition Nutrition Support Monitoring Guidelines in the Stable Dialysis Patient Intraperitoneal Amino Acids as Nutrition Support in PD Clinical Associations with Negative Nitrogen Balance/Estimation of Nitrogen Balance

© 2005 National Kidney Foundation, Inc. All Rights Reserved

8-13 8-14 8-15 8-16 8-17 8-17 8-18 8-19 8-20 8-21 8-22 8-23 8-24

9-2 9-3 9-4 9-5 9-6 9-7 9-8 9-9 9-10 9-11 9-12 9-13 9-14 9-15 9-16 9-17 9-18 9-19 9-20 9-21 9-22

4

Pocket Guide to Nutrition Assessment of the Patient with Chronic Kidney Disease Chapter 10: Adequacy of Dialysis and Urea Kinetic Modeling General Information K/DOQI Suggested Adequacy Targets, 2001 Kinetic Modeling Glossary Methods of Measuring Hemodialysis Adequacy Parameters That Affect Adequacy Formal Urea Kinetic Modeling (Kt/V) Components Body Water Volume Volume From Surface Area (VSA) Calculation Formulas Differences Between Single Pool and Double Pool Kinetics Hemodialysis Formulas for Urea Kinetic Modeling (UKM) Summary of K/DOQI Hemodialysis Adequacy Recommendations Common Causes of Delivered Kt/V Unequal to Prescribed Steps to Error Analysis of Formal HD UKM Helpful Information for Analysis of UKM Results Error Analysis for Formal UKM Dialyzer Characteristics Formulas to Estimate Equilibrated Kt/V Formulas for Other Measures of Adequacy Daily Hemodialysis Peritoneal Dialysis Adequacy Formulas Summary of K/DOQI PD Adequacy Guidelines Kinetic Modeling Formulas for CKD Not on Dialysis Nutrition Intervention Based on nPNA Glomerular Filtration Rate Calculations

10-2 10-2 10-3 to 10-5 10-6 10-7 10-7 10-8 10-9 10-10 10-11 10-12 10-13 10-14 10-15 10-16 to 10-18 10-19 10-20 10-21 10-22 10-23 to 10-24 10-25 10-26 10-27 10-28

Chapter 11: Special Considerations for the Pediatric Patient with CKD Note Page Nutrition Assessment of the Pediatric Patient Practical Steps to Nutrition Assessment of Pediatric Patients Assessment of Protein/Energy Status in Pediatric Patients Mid-Arm Circumference (MAC) Reference Values Triceps Skinfold Thickness Estimated Mid-Arm Muscle Circumference Formula for Mid-Arm Muscle Circumference and Area Formulas for Calculating Standard Deviation Scores 50th Percentile for Height in Boys/Standard Deviation Values for Height in Boys 50th Percentile for Height in Girls/Standard Deviation Values for Height in Girls 50th Percentile for Weight in Boys/Standard Deviation Values for Weight in Boys 50th Percentile for Weight in Girls/Standard Deviation Values for Weight in Girls Pediatric Laboratory Values That Are Different From Adult Values Estimating Calorie and Fluid Needs of Pediatric CKD Patients Guidelines for Choosing an Infant Formula Pediatric Formulas Used in CKD

11-2 11-3 11-4 11-5 11-6 11-7 11-8 11-9 11-9 11-10 to 11-11 11-12 to 11-13 11-14 to 11-15 11-16 to 11-17 11-18 11-19 11-20 11-21

© 2005 National Kidney Foundation, Inc. All Rights Reserved

5

Pocket Guide to Nutrition Assessment of the Patient with Chronic Kidney Disease Chapter 11: Special Considerations for the Pediatric Patient with CKD (cont.) Average Number and Volume of Feedings for an Infant Without CKD Nutrient Recommendations for Pediatric Patients (ARF, CKD, HD, PD, Transplant) Bone Abnormalities in Pediatric Patients with CKD Malnutrition in Pediatric Patients with CKD Guidelines for Enteral Feedings in Pediatric Patients with CKD Guidelines for Tube Feedings in Pediatric Patients with CKD Guidelines for Parenteral Nutrition in Pediatric Patients with CKD Guidelines for Urea Kinetic Modeling in Pediatric HD Patients Guidelines for Adequacy Testing in Pediatric PD Patients Calcium Urolithiasis/Hyperoxaluria Pediatric References

© 2005 National Kidney Foundation, Inc. All Rights Reserved

11-21 11-22-11-26 11-27 11-28 11-29 11-30 11-31 11-32 11-33 11-34 11-34

6

Chapter 1: NUTRITION ASSESSMENT CHARTS, TABLES, AND FORMULAS

PRACTICAL STEPS TO NUTRITION ASSESSMENT-ADULT PATIENTS 1.

Review the medical history (concurrent diseases, drug/nutrient interactions, hospitalizations, weight changes, comparison of current weight to usual and standard, conditions that interfere with ingestion/absorption/mastication/elimination). 2. Diet history including “normal” for the patient and changes in appetite or intake, food intolerances, pica behavior, religious diet restrictions, past diet modifications and instruction, patient’s understanding of diet and disease, educational level, patient’s perspective of weight changes, food preferences, use of salt and sugar, food allergies, typical meal pattern/food frequency record, use of supplements, urine output, physical/economic/psychological problems, family/other support, activity level, and sleep patterns. 3. Anthropometric measurements/physical examination: measured height, frame size, weight, subjective global assessment, arm anthropometrics (triceps skinfold, mid-arm muscle circumference Page 1-27 to 1-32), and general appearance. (Subjective Global Assessment: Page 1-34 to 1-41). 4. Review of chemistries look for values that identify areas of concern (nutrition/immune status, state of uremia, bone status, electrolyte status, iron status, vitamin/mineral status, hydration status, glycemic control). 5. Assess current intake Kcal, carbohydrate, protein, fat, Na+, K+, Ca++, P, fluid, vitamins, minerals. 6. Assess/develop nutrition problem list with prioritized interventions. 7. Develop individualized diet prescription/meal pattern with appropriate diet modifications for nutrition problems and individual preferences. Be as liberal as possible to promote adequate intake and good nutrition status. 8. Instruct patient/other; provide written materials at predetermined level of education/understanding. 9. Follow-up within one to three months to assess appropriateness of diet modification as well as patient satisfaction and understanding. Modify plan as appropriate. 10. Reevaluate on a regular basis whenever the patient has a change in status such as significant weight change, extended hospitalization, or acute illness. 1-2

K/DOQI ASSESSMENT AND MONITORING RECOMMENDATIONS:

Parameter

Frequency

Serum albumin

Monthly

nPNA

At least: monthly-HD; every 4 months-PD

% Usual dry weight (post dialysis or post-drain)

Monthly

% Standard body weight

Every 4 months

Subjective Global Assessment

Biannually

Diet interview/diary

Biannually

Anthropometrics, DEXA, Prealbumin, Creatinine

As needed

Index, Creatinine, Urea Nitrogen, Cholesterol

Adapted from: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

TIPS FOR EFFECTIVE ASSESSMENT, INTERVIEWING, AND TEACHING •

Introduce yourself.

•

Make eye contact and use a receptive posture.

•

Explain what you will be doing.

•

Assess prior learning.

•

Gear information to the individual’s knowledge and education.

•

Ask open-ended questions without leading responses.

•

Utilize food models or other references to enhance accuracy of patient responses.

•

Acknowledge patient responses.

•

Limit the time spent and the volume of information given at each session.

•

Give written material to reinforce verbal instructions.

•

Identify and use patient-specific motivational factors.

•

Encourage the patient to participate in his or her own nutritional care and to ask questions.

HEIGHT ESTIMATION FROM KNEE HEIGHT Knee height is highly correlated with stature and may be used to estimate height in persons who are unable to stand. Use a knee height caliper with the knee bent at a 90-degree angle while the patient is in a supine position. Measure the distance from the heel to the top of the knee on the outside of the left leg (or the nonaccess leg). Take two successive measurements. They should agree within 5 mm. Male height (cm) = (2.02 x knee height cm) - (0.04 x age) + 64.19 Female height (cm) = (1.83 x knee height cm ) - (0.24 x age) + 84.88 Reference: Chumlea WC, Roche AF: Nutritional Assessment of the Elderly through Anthropometry, Ross Laboratories, Columbus, Ohio, 1987

1-5

HEIGHT ESTIMATION FROM ARM SPAN Arm span is approximately equal to height (within 10% error) in both men and women, although it usually slightly overestimates height. With the arms fully extended and parallel to the ground, measure the distance from the tip of the middle finger on one hand to the tip of the middle finger on the other hand. It may be easiest to measure across the patient’s back. References:

Clinical Geriatrics, Lippincot Co. Philadelphia, PA, 1979 Simko M, et al: Nutrition Assessment - A Comprehensive Guide for Planning Intervention, ASPEN Publications, 1995

1-6

DETERMINATION OF FRAME SIZE BY ELBOW BREADTH (K/DOQI) 1.

Have the patient stand, facing you with feet together. Ask him or her to extend the right arm in front of the body with the forearm at a 90-degree angle, the inside of arm facing the body, and the fingers pointing up.

2.

Place the thumb and index finger (or calipers with blades up) against the two prominent bones on either side of the elbow, exert firm pressure to minimize influence of soft tissue, measure the distance between your thumb and index finger or the caliper blades. Take the reading while the arm is still bent and in the caliper and measure to the nearest 0.1 cm. Measure twice and use the average of the two measurements.

3.

Determine the frame size using the patient’s height and elbow breadth on the chart below. Use frame size to determine standard or ideal body weight.

Age 18 - 24 25 - 34 35 - 44 45 - 54 55 - 64 65 - 74

Small ≤6.6 ≤6.7 ≤6.7 ≤6.7 ≤6.7 ≤6.7

Male Medium >6.6 and <7.7 >6.7 and <7.9 >6.7 and <8.0 >6.7 and <8.1 >6.7 and <8.1 >6.7 and <8.1

Large ≥7.7 ≥7.9 ≥8.0 ≥8.1 ≥8.1 ≥8.1

Small ≤5.6 ≤5.7 ≤5.7 ≤5.7 ≤5.8 ≤5.8

Female Medium >5.6 and <6.5 >5.7 and <6.8 >5.7 and <7.1 >5.7 and <7.2 >5.8 and <7.2 >5.8 and <7.2

Large ≥6.5 ≥6.8 ≥7.1 ≥7.2 ≥7.2 ≥7.2

Adapted from: Frisancho AR: New standards of weight and body composition by frame size and height for assessment of nutritional status of adults and the elderly. Am J Clin Nutr 40: 808-819, 1984 1-7

DETERMINATION OF FRAME SIZE BY WRIST CIRCUMFERENCE Use a fiberglass tape to measure the circumference of the right (or nonaccess) wrist just beyond the wrist bone toward the hand. If the right wrist is swollen or enlarged for any reason, use the left wrist. Note which wrist is measured (for subsequent measurements) and record the measurement in cm. Frame Size

=

__Height (cm)___ Wrist circumference (cm)

CONVERSION TABLE

Males >10.5 9.6 - 10.5 <9.6

Frame Size Small Medium Large

Females >11.0 10.1 - 11.0 <10.1

Reference: Gant JP: Handbook of Parenteral Nutrition, W.B. Saunders, Philadelphia, 1980

1-8

PATIENT-DETERMINED FRAME SIZE For a patient-determined frame size, have the patient encircle the non-dominant wrist with the thumb and index finger of the dominant hand at the level of the radius and ulnar styloid process. Note whether the thumb and index finger overlap, meet, or do not meet. This method is not precise.

Frame Size Small Medium Large

Indicator Thumb and index finger overlap Thumb and index finger meet or touch Thumb and index finger do not meet or touch

Reference: Page CP, et al: Nutritional Assessment and Support - A Primer 2nd Edition, Williams & Wilkins, Baltimore, 1994

METHODS TO DETERMINE BODY WEIGHTS FOR NUTRIENT CALCULATIONS 1.* Standard Body Weight: Median body weight of normal Americans of the same height, gender, skeletal frame size, and age range from the NHANES II data. (K/DOQI) (Page 1-11) 2.* Adjusted Body Weight: Use for obese or lean patients who are <95% or 115% standard body weight. (K/DOQI) (Page 1-19 for formula). 3. Desirable Body Weight - Metropolitan Life Insurance Height and Weight Tables for Adults, 1983 (Pages 1-12 to 1-13) 4. Hamwi method - Not recommended; based on older NHANES data.

*K/DOQI Clinical Practice Guidelines for Nutrition in CRF recommend that standard and adjusted body weights, #1 and # 2 above, be used to calculate nutrient levels. Some of the categories within the NHANES standard body weight table were determined with small numbers of patients or linear regression and may be inappropriate for an individual patient. Clinical judgment and longitudinal assessment of body weight should be utilized with other nutrition measures to assess response to nutrition therapy and to make adjustments. Adoption of a consistent method of determining body weight will simplify comparison of data and research within the renal community. References:

Simko M, et al: Nutrition Assessment: A Comprehensive Guide for Planning Interventions ASPEN, 1995 Alpers D, Stenson W, Bier D: Manual of Nutritional Therapeutics, Lippincott, Williams & Wilkins, 2002 Kopple JD, et al: Proposed Glossary for Dialysis Kinetics. Am J Kidney Dis 26(6):963-981, 1995 NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

STANDARD BODY WEIGHT (K/DOQI) NHANES II – Average 50th percentile weights for men and women by age, height, and frame size in the US. Note: Some categories are based on a small sample of patients or estimated with linear regression and may not be appropriate for an individual patient. Use clinical judgment in applying these standard body weights. Frame (Htcm)

Male/age S

25 - 54 years M L

S

55 - 74 years M L

Frame (Htcm)

157

64

68

82

61

68

160

61

71

83

62

163

66

71

84

165

66

74

168

67

170

Female/age S

25 - 54 years M L

S

55 - 74 years M L

77*

147

52

63

86

54

57

92

70

80

150

53

66

78

55

62

78

63

71

77

152

53

60

87

54

65

78

79

70

72

79

155

54

61

81

56

64

79

75

84

68

74

80

157

55

61

81

58

64

82

71

77

84

69

78

85

160

55

62

83

58

65

80

173

71

78

86

70

78

83

163

57

62

79

60

66

77

175

74

78

89

75

77

84

165

60

63

81

60

67

80

178

75

81

87

76

80

87

168

58

63

75

68

66

82

180

76

81

91

69

84

84

170

59

65

80

61*

72

80

183

74

84

91

76*

81

90

173

62

67

76

61*

70

79

185

79*

85

93

78*

88

88

175

63*

68

79

62*

72*

85*

188

80*

88

92

77*

95

89

178

64*

70

76

63*

73*

85*

*Estimated with linear regression formula Reference: Frisancho AR: New Standards of weight and body composition by frame size and height for assessment of nutritional status of adults and the elderly. Am J Clin Nutr 40:808-819, 1984 1-11

METROPOLITAN LIFE HEIGHT AND WEIGHT TABLES FOR ADULTS, 1983 MALES, Ages 25-59 Height feet 5' 1" 5' 2” 5' 3" 5' 4" 5' 5" 5' 6" 5' 7" 5' 8" 5' 9" 5' 10" 5' 11" 6' 0 6' 1" 6' 2" 6' 3"

cm 154.9 157.5 160.0 162.6 165.1 167.6 170.2 172.7 175.3 177.8 180.3 182.9 185.4 188.0 190.5

Small Frame lbs kg 128-134 58.2-60.9 130-136 59.1-61.8 132-138 60.0-62.7 134-140 60.9-63.6 136-142 61.8-64.5 138-145 62.7-65.9 140-148 63.6-67.2 142-151 64.5-68.6 144-154 65.5-70.0 146-157 66.4-71.4 149-160 67.7-72.7 152-164 69.1-74.5 155-168 70.5-76.4 158-172 71.8-78.2 162-176 73.6-80.0

Medium Frame lbs kg 131-141 59.5-64.1 133-143 60.4-65.0 135-145 61.4-65.9 137-148 62.3-67.2 139-151 63.2-68.6 142-154 64.5-70.0 145-157 65.9-71.4 148-160 67.2-72.7 151-163 68.6-74.1 154-166 70.0-75.5 157-170 71.4-77.3 160-174 72.7-79.1 164-178 74.5-80.9 167-182 75.9-82.7 171-187 77.7-85.0

Large Frame lbs kg 138-150 62.7-68.2 140-153 63.6-69.5 142-156 64.5-70.9 144-160 65.5-72.7 146-164 66.4-74.5 149-168 67.7-76.4 152-172 69.1-78.2 155-176 70.5-80.0 158-180 71.8-81.8 161-184 73.2-83.6 164-188 74.5-85.5 168-192 76.4-87.3 172-197 78.2-89.5 176-202 80.0-91.8 181-207 82.3-94.1

Reprinted with permission. Height is without shoes. Weight includes indoor clothing-5lbs. (Light- weight pants/ T-shirt = 2 lbs, Sweatshirt/Jeans = 3.5 lbs, Sweatsuit/T-Shirt = 3 lbs.)

1-12

METROPOLITAN LIFE HEIGHT AND WEIGHT TABLES FOR ADULTS, 1983 FEMALES, Ages 25-59 Height feet 4' 9” 4'10" 4'11" 5' 0 5' 1" 5' 2" 5' 3" 5' 4" 5' 5" 5' 6" 5' 7" 5' 8" 5' 9" 5' 10" 5' 11"

cm 144.8 147.3 149.9 152.4 154.9 157.5 160.0 162.6 165.1 167.6 170.2 172.7 175.3 177.8 180.3

Small Frame lbs kg 102-111 46.4-50.0 103-113 46.8-51.4 104-115 47.3-52.3 106-118 48.2-53.6 108-121 49.1-55.0 111-124 50.5-56.4 114-127 51.8-57.7 117-130 53.2-59.0 120-133 54.5-60.5 123-136 55.9-61.8 126-139 57.3-63.2 129-142 58.6-64.5 132-145 60.0-65.9 135-148 61.4-67.3 138-151 62.7-73.6

Medium Frame lbs kg 109-121 49.5-55.0 111-123 50.0-55.9 113-126 51.4-57.2 115-129 52.3-58.6 118-132 53.5-60.0 121-135 55.0-61.4 124-138 56.4-62.7 127-141 57.7-64.1 130-144 59.0-65.5 133-147 60.5-66.8 136-150 61.8-68.2 139-153 63.2-69.5 142-156 64.6-70.9 145-159 65.9-72.3 148-162 67.3-73.6

Large Frame lbs kg 118-131 53.6-59.5 120-134 54.5-60.9 122-137 55.5-62.3 125-140 56.8-63.6 128-143 58.2-65.0 131-147 59.5-66.8 134-151 60.9-68.6 137-155 62.3-70.5 140-159 63.6-72.3 143-163 65.0-74.1 146-167 66.4-75.9 149-170 67.7-77.3 152-173 69.1-78.6 155-176 70.5-80.0 158-179 71.8-81.4

Reprinted with permission. Height is without shoes. Weight includes indoor clothing 2-5 lbs. (Light-weight pants/T-shirt = 2 lbs, Sweatshirt/Jeans = 3.5 lbs, Sweatsuit/T-Shirt = 3 lbs.)

1-13

WEIGHT FOR HEIGHT TABLES FOR FILIPINOS (Ages 25-65) Htcm 140 141 142 143 144 145 146 147 148 149 150 151 152 153 154 155 156 157 158 159 160

Male Wtkg 34.4-42.0 35.1-42.8 35.8-43.7 36.5-44.6 37.2-45.4 37.9-46.3 38.6-46.2 39.3-48.0 40.0-48.9 40.7-49.7 41.4-50.6 42.1-51.5 42.8-52.3 43.5-53.2 44.2-54.0 44.9-54.9 45.6-55.8 46.3-56.3 47.0-57.5 47.8-58.4 48.4-59.2

Htcm 161 162 163 164 165 166 167 168 169 170 171 172 173 174 175 176 177 178 179 180 181

Wtkg 49.1-60.1 49.9-60.9 50.6-61.8 51.3-62.7 52.0-63.5 52.7-64.4 53.4-65.2 54.1-66.1 54.8-67.0 55.5-67.8 56.2-68.7 56.9-69.6 57.6-70.4 58.3-71.3 59.0-72.1 59.7-73.0 60.4-73.9 61.1-74.7 61.8-75.6 62.6-76.4 63.2-77.3

Htcm 129 130 131 132 133 134 135 136 137 138 139 140 141 142 143 144 145 146 147 148 149

Female Wtkg Htcm 29.5-36.0 150 30.1-36.3 151 30.7-37.5 152 31.3-38.2 153 31.9-38.9 154 32.5-39.7 155 33.1-40.4 156 33.6-41.4 157 34.2-41.8 158 34.8-42.6 159 35.4-43.3 160 36.0-44.0 161 36.6-44.8 162 37.2-45.5 163 37.8-46.2 164 38.4-47.3 165 39.0-47.6 166 39.6-48.4 167 40.2-49.1 168 40.8-49.8 169 41.4-50.5 170

Wtkg 41.9-51.3 42.6-52.0 43.1-52.7 43.7-53.4 44.3-54.1 44.9-54.9 45.5-55.6 46.1-56.4 46.7-57.1 47.3-57.8 47.9-58.5 48.5-59.3 49.1-60.0 49.7-60.7 50.3-61.4 50.8-62.2 51.4-62.9 52.0-63.6 52.6-64.3 53.2-65.0 53.8-65.8

Reference: (Adapted) Nutritionist-Dietitian’s Association of the Philippines, Diet Manual, 4th Ed. 1994 1-14

DESIRABLE BODY WEIGHT BASED ON BMI Weight tables are not readily available for all cultures or nationalities. In addition, the standard weight tables for the U.S. population often seem inappropriate for those from other countries or cultures. Since BMI is used in many countries to assess “desired” weight, the table below provides weights for BMI from 20-25 and for BMI from 23.6-24 (suggested as the best range for survival in HD patients).1 The clinician should compare these ranges to the “normal” adult weight as a way of determining a “desired” weight that is reasonable for the individual patient.

Height in/cm 53/134.6

Wt Range kg BMI 20-25 36.2-45.3

Wt Range kg BMI 23-24 41.7-43.5

Height in/cm 66/167.6

Wt Range kg BMI 20-25 56.2-70.3

Wt Range kg BMI 23-24 64.6-67.3

54/137.2

37.6-47.0

43.3-45.2

67/170.2

57.9-72.4

66.6-69.5

55/139.7

39.0-48.8

44.9-46.8

68/172.7

59.7-74.6

68.6-71.6

56/142.2

40.5-50.6

46.5-48.6

69/175.3

61.4-76.8

70.6-73.7

57/144.8

41.9-52.4

48.2-50.3

70/177.8

63.2-79.0

72.7-75.9

58/147.3

43.4-54.3

49.9-52.1

71/180.3

65.0-81.3

74.8-78.1

59/149.9

44.9-56.1

51.7-53.9

72/182.9

66.9-83.6

76.9-80.3

60/152.4

46.5-58.1

53.4-55.7

73/185.4

68.8-86.0

79.1-82.5

61/154.9

48.0-60.0

55.2-57.6

74/188.0

70.7-88.3

81.3-84.8

62/157.5

49.6-62.0

57.0-59.5

75/190.5

72.6-90.7

83.5-87.1

63/160.0

51.2-64.0

58.9-61.5

76/193.0

74.5-93.2

85.7-89.4

64/162.6

52.9-66.1

60.8-63.4

77/195.6

76.5-95.6

88.0-91.8

65/165.1

54.5-68.1

62.7-65.4

78/198.1

78.5-98.1

90.3-94.2

References:

1

Kopple JD, Zhu X, Lew NL, Lowrie EG: Body weight for height relationships predict mortality in maintenance hemodialysis patients. KI 56:1136-1148, 1999 Alpers D, Stenson W, Bier D: Manual of Nutritional Therapeutics, Lippincott, Williams, Wilkins, 2002 1-15

ESTIMATING DRY WEIGHT 142 mEq/L X Liters of NTBW Pre-dialysis serum sodium (mEq/L)

=

Liters of actual body water

142 mEq/L = normal state of hydration NTBW = Normal Total Body Water is calculated by multiplying the patient’s pre-dialysis weight by the average percentage of body water for males (60%) and females (50%). A lower value (males - 57% and females 47%) should be used in muscle wasted or overweight dialysis patients. Example:

Male, pre-dialysis weight of 63 kg, serum sodium of 131 mEq/L, and low muscle stores.

63 x 0.57 = 35.91 142 mEq/L x 35.91 = 5099.22 = 38.9 (Actual TBW) 131 mEq/L 131 38.9-35.9 = 3 kg excess body fluid 63 kg - 3.0 kg = 60.0 kg Estimated Dry Weight (This formula does not consider fluid in tissues, so can only be used as one aspect of assessing dry weight). Reference: Smith, et al. Formulation of Dry Weight Calculation. Contemp Dial & Nephr, May, 1990 1-16

CLINICAL SIGNS OF FLUID STATUS IN DIALYSIS PATIENTS Fluid Overload Gain >4% body weight between treatments Hypertension (onset or increase in BP) Peripheral edema, ascites, pleural effusion Left ventricular failure with rales in lungs, labored breathing while supine, third heart sound Dilution of the serum can cause some laboratory values to be falsely low

Dehydration Minimal weight gain/weight loss between treatments Hypotension/orthostatic fall in blood pressure Collapsing veins/difficult venipuncture Cool extremities Decreased skin turgor

Concentration of the serum can cause some laboratory values to be falsely high

USUAL FLUID INTAKE AND OUTPUT IN ADULTS WITHOUT KIDNEY DISEASE

Intake Fluid ingestion: about 1000 to 2000 cc/day (Influenced by salt intake/eating patterns) Fluid from solid foods: 800-1000 cc/day Oxidative metabolism: 200 to 300 cc/day

Output Urine: normal 1000-2000 cc/day; varies to maintain fluid balance; decreases to negligible in CKD Perspiration: minimal except in hot climate Evaporation: 450 cc/day each from skin/respiration Stool: approximately 100 cc/day

Reference: Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997 1-17

WEIGHT COMPARISON FORMULAS Percent Standard Body Weight (% SBW) (K/DOQI) Percent Desirable Body Weight (% DBW) Percent Usual Body Weight (% UBW) Percent Weight Change (% Wt Change)

Actual Body Weight x 100 Standard Body Weight (See page 1-11) Actual Body Weight x 100 Desirable Body Weight (See pages 1-12 and 1-13) Actual Body Weight x 100 Usual Weight (Previous Weight - Actual Weight) x 100 Previous Weight

Standard body weight may also be called “Relative” body weight 1 Reference: Kopple JD, et al: A proposed glossary for dialysis kinetics. Am J Kidney Dis 26(6):963-981, 1995

1-18

Adjusted body weight for the obese or Underweight Patient* (K/DOQI) 1 Adjusted body weight (BW)= edema-free BW + [(standard BW - edema-free BW) x 0.25] *Adjust when patient’s weight is < 95% or >115% of standard body weight (page 1-11).

Examples of K/DOQI adjustment: Underweight patient: Actual BW 60, Standard BW 80 so Adjusted BW = 60 + [(80 - 60) x 0.25] Adjusted BW = 60 + [20 x 0.25] Adjusted BW = 60 + 5 or 65 (Traditional adjustment = not applied to underweight patients) Overweight patient: Actual BW 80, Standard BW 60 so Adjusted BW = 80 + [(60-80) x 0.25] Adjusted BW = 80 + [-20 x 0.25] Adjusted BW = 80 - 5 or 75 (Traditional adjustment = 65) The K/DOQI adjustment is less extreme than the traditional adjustment with the rationale that patient compliance might be enhanced with more modest step-wise alterations in nutrient intake. Thus, the K/DOQI adjusted weight is used to calculate a starting point for nutrient levels, but requires periodic reassessment of weight and recalculation of needs as the patient’s status changes. As part of the recommended research in the nutrition guidelines, renal clinicians are asked to utilize and test the K/DOQI formulas to validate their accuracy and usefulness. Traditional Adjustment2: Adjusted BW = IBW + [(Actual BW - Ideal BW x 0.25)] The originally published adjustment formula as was developed for obese individuals (>125% of ideal BW) with the understanding that fatty tissue is less metabolically active than lean tissue and requires different nutrient levels for maintenance. Thus, nutrient recommendations based on actual BW were likely to overestimate needs and those based on ideal BW might underestimate the needs of an obese individual. There was no application of the traditional formula to underweight patients since the research focussed on obese patients. In the past, renal clinicians have recommended nutrient levels based on ideal weight for underweight patients. Regardless of the formula employed, clinicians must consider the appropriateness of the adjustment for an individual patient. Reference:

1 2

NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure, Am J Kidney Dis 35 (6) Suppl 2, June, 2000 Karkeck J. Adjustment for Obesity. ADA Renal Practice Group Newsletter, Winter, 3(1):6,1984

1-19

WEIGHT ESTIMATION IN AMPUTEES To estimate the weight of persons with amputations for comparison to SBW (Page 1-11): To estimate the preamputation BW, increase the post amputation BW by the percentage listed for the amputated appendage(s). Example: Post-amputation BW is 62.2 kg with one below the knee (BK) amputation. 62.2 kg x 6.5% = 4.0 kg 4.0 kg to 62.2 = 66.2 (Underestimation due to use of post-amputation BW to calculate % lost) To estimate the post-amputation BW, reduce pre-amputation BW by the % listed for the amputated appendage(s). Example: Pre-amputation weight is 67 with one BK amputation. 67 kg x 6.5% = 4.4 kg 67 kg - 4.4 kg = 62.6 kg To estimate volume (V) change after amputation: Post-amputation BW X pre-amputation V/pre-amputation BW Example: Post-amputation BW = 62.2, pre-amputation V = 56, pre-amputation BW = 67 56/67 kg = 0.84 62.2 kg x 0.84 = 52.2 L (Assumes body water content does not change with amputation).

Upper Body Head, neck, trunk Hand Forearm + hand Entire arm

% BW 49.7 0.8 3.1 6.6

% BSA C 2.5 6 10

Lower Body Foot Lower leg, below knee Leg, above knee Entire leg

% BW 1.8 6.5 8.0 18.5

% BSA 3.5 10 12.5 18 1-20

BODY MASS INDEX (BMI) (K/DOQI) 1. Standard Formula BMI =

Weight (kg) Height (m2)

Conversion to M2 Height M2 Height Feet /cm Feet /cm / 144.8 cm 2.10 5’7" / 170.2 cm 4’9" 4’10" / 147.3 cm 2.17 5’8" / 172.7 cm 4’11" / 149.9 cm 2.25 5’9" / 175.3 cm / 152.4 cm 2.32 5’10" / 177.8 cm 5' / 154.9 cm 2.40 5’11" / 180.3 cm 5’1" / 182.9 cm 6' / 157.5 cm 2.48 5’2" / 160.0 cm 2.56 6’1" / 185.4 cm 5’3" / 162.6 cm 2.64 6’2" / 188.0 cm 5’4" / 165.1 cm 2.73 6’3" / 190.5 cm 5’5" / 167.6 cm 2.81 6’4" / 193.0 cm 5’6" Reference:

2. Simplified BMI =

2

M

2.90 2.98 3.07 3.16 3.25 3.35 3.44 3.53 3.63 3.73

Height Inches/Feet / 4’9" 57" / 4’10" 58" / 4’11" 59" / 5’0" 60" / 5’1" 61" / 5’2" 62" / 5’3" 63" / 5’4" 64" / / 5’5" 65" 5’6" 66"

Weight (lbs) x 705 Height (in2)

Conversion to Inches2 In2 Height Inches/Feet / 5’7" 67" 3249 / 5’8" 68" 3364 / 5’9" 69" 3481 70" / 5’10" 3600 71" / 5’11" 3721 / 6’0" 72" 3844 / 6’1" 73" 3969 / 6’2" 74" 4096 / 6’3" 75" 4225 / 6’4" 76" 4356

In2 4489 4624 4761 4900 5041 5184 5329 5476 5625 5776

Stensland SH, et al: Simplifying the calculation of body mass index for quick reference. J of Am Dietetic Assoc. 90 (6):856, 1990

1-21

BODY MASS INDEX CLASSIFICATIONS BMI Under 20 20 - 25 25 - 27 Over 27 K/DOQI

References:

Evaluation May be associated with health problems and malnutrition. “Ideal” index range associated with the lowest risk of illness in people without kidney disease. May be associated with health problems related to overweight in some persons. Associated with increased risk of health problems related to obesity such as heart disease, high blood pressure, and diabetes. 23.6 for women and 24.0 for men Note: Upper 50th percentile BMI may be best for survival in maintenance dialysis (MD) patients. MD patients who are over 120% SBW or BMI >30 may benefit from weight reduction, but the safety and efficacy of nutrient modification for weight loss needs to be studied. Classifications of Body Mass Index by Health and Welfare. Canada, 1988 NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure, Am J Kidney Dis 35(6) Suppl 2, June, 2000

1-22

CREATININE INDEX (For estimating edema-free lean body mass): The creatinine (Cr) index is defined as the creatinine synthesis or production rate and is used to assess skeletal muscle mass. It is determined by the size of the skeletal muscle mass and the intake of creatine and creatinine. Creatinine production is approximately proportional to skeletal muscle mass in metabolically stable adults who have consistent protein intake. In MD patients creatinine is synthesized and serum levels rise at a rate that is approximately proportional to somatic protein mass and dietary protein intake. The creatinine index is measured as the sum of creatinine removed from the body (urine, dialysate, ultrafiltrate), any increase in the body creatinine pool, and the creatinine degradation rate. *Creatinine Index mg/24 hr = dialysate (ultrafiltrate) Cr mg/24 hr + urine Cr mg/24 hr + change in Cr body pool mg/24 hr + Cr degradation mg/24 hr Change in body creatinine pool mg/24 hr = (Final serum Cr mg/L - initial serum Cr) x (24 hour/time interval between creatinine measurements) x (BW kg x 0.5 L/kg) If body weight is variable: Change in body creatinine pool mg/24 hr = [final serum Cr mg/L x (final BW kg x 0.5 L/kg)] - [initial serum Cr mg/L x (initial BW kg x 0.5 L/kg)] x (24 hr/time interval between creatinine measurements) Creatinine Degradation (gut) mg/24 hr = 0.038 dL/kg/24 hr x serum Cr mg/dL x BW kg Edema-free lean body mass kg = 0.029 kg/mg/24 hr x Cr index mg/24 hr + 7.38 kg *(Creatinine Index or Total creatinine production = creatinine excretion + creatinine degradation - See next page) Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure, Am J Kidney Dis 35(6) Suppl 2, June, 2000 1-23

SAMPLE CALCULATION OF EDEMA-FREE LEAN BODY MASS PD Patient: Urine Volume = 475 Effluent Volume = 12485 Serum Cr = 6.91 BW = 70.6 Cr degradation (gut)

Urine Creatinine mg/mL = 136 Effluent Creatinine mg/mL = 4.5

= 0.038 x (Scr x Wtkg) = 0.038 x 6.91 x 70.6 = 18.6 mg/d

Cr production

= = = =

Dcr x (Dv/100) + Ucr x (Uv/100)/1000 4.5 x (12485/100) + 136 x (475/100) 562 + 646 1208 mg/d

Creatinine Index (Total creatinine production) = 1208 + 18.6 or 1226.6 mg/d Edema Free LBM = 0.029 x 1226.6 + 7.38 or 42.95 kg Edema Free LBM = 61% of total weight is LBM

1-24

BODY SURFACE AREA NOMOGRAM Wt Kg/Lbs 38.6 40.9 43.2 45.5 47.7 50.0 52.3 54.6 56.8 59.1 61.4 63.6 65.9 68.2 70.5 72.7 75.0 77.3 79.6 81.8 86.4 90.9

Ht 58”

85 90 95 100 105 110 115 120 125 130 135 140 145 150 155 160 165 170 175 180 190 200

1.27 1.30 1.33 1.36 1.39 1.41 1.44 1.47 1.49 1.52 1.54 1.57 1.59 1.61 1.63 1.66 1.68 1.70 1.72 1.74 1.78 1.82

60”

62”

64”

66”

68”

1.30 1.33 1.36 1.39 1.42 1.45 1.48 1.50 1.53 1.55 1.58 1.60 1.63 1.65 1.68 1.70 1.72 1.74 1.76 1.79 1.83 1.87

1.33 1.36 1.39 1.42 1.45 1.48 1.51 1.54 1.57 1.59 1.62 1.64 1.67 1.69 1.72 1.74 1.76 1.78 1.81 1.83 1.87 1.91

1.36 1.39 1.43 1.46 1.49 1.52 1.55 1.57 1.60 1.63 1.66 1.68 1.71 1.73 1.76 1.78 1.80 1.83 1.85 1.87 1.91 1.96

1.39 1.43 1.46 1.49 1.52 1.55 1.58 1.61 1.64 1.67 1.69 1.72 1.75 1.77 1.80 1.82 1.84 1.87 1.89 1.91 1.96 2.00

1.42 1.46 1.49 1.52 1.55 1.59 1.62 1.65 1.67 1.70 1.73 1.76 1.78 1.81 1.83 1.86 1.88 1.91 1.93 1.96 2.00 2.04

70” 1.45 1.49 1.52 1.56 1.59 1.62 1.65 1.68 1.71 1.74 1.77 1.79 1.82 1.85 1.87 1.90 1.92 1.95 1.97 2.00 2.04 2.09

72”

74”

76”

1.48 1.52 1.55 1.59 1.62 1.65 1.68 1.72 1.75 1.77 1.80 1.83 1.86 1.89 1.91 1.94 1.96 1.99 2.01 2.04 2.09 2.13

1.51 1.55 1.58 1.62 1.65 1.69 1.72 1.75 1.78 1.81 1.84 1.87 1.90 1.92 1.95 1.98 2.00 2.03 2.05 2.08 2.13 2.17

1.54 1.58 1.62 1.65 1.69 1.72 1.75 1.78 1.82 1.85 1.88 1.90 1.93 1.96 1.99 2.02 2.04 2.07 2.09 2.12 2.17 2.22

Reference: Baxter Healthcare Training Seminar, Chicago, 1991 1-25

BODY SURFACE AREA (BSA) FORMULAS 1

Dubois and Dubois : BSA (m2) = 0.007184 X BW (kg)0.425 X Height (cm)0.725 Gehan and George2: BSA (m2) = 0.0235 X Weight (kg)0.51456 X Height (cm)0.42246 Haycock3: (Pediatrics) BSA (m2) = 0.024265 X Height (cm)0.3964 X Weight (kg)0.5378 Mosteller5: BSA (m2) = ([Ht(cm) X Wt(kg)]/3600)1/2 References:

BSA Adjustment for Amputation Part of Body % Wt Loss % BSA4 Arm at shoulder 6.6 10.0 Arm at elbow 3.1 6.0 Hand alone 0.8 2.5 Leg at hip 18.5 18.0 Leg above knee 8.0 12.5 Leg below knee 6.5 10.0 Foot alone 1.8 3.5

1. Dubois D, Dubois AEF: A formula to estimate the approximate surface area if height and weight be known. Nutrition 5:303-311, 1989 2. Gehan E, George SL: Estimation of human body surface area from height and weight. Cancer Chemother Rep Part I 54:225235, 1970 3. Haycock GB, Chir B, Schwartz, et al: Geometric method of for measuring body surface area: A height-weight formula validated in infants, children, and adults. J Pediatr 93:62-66, 1978 4. Tzamaloukas AH, Malhotra D: CrCl in amputees on CPD. Perit Dial Int 16:426, 1996 5. Mosteller RD: Simplified Calculation of BSA. N Eng J Med, 22;317(17):1098, 1987

1-26

ARM ANTHROPOMETRICS Step I Mid-arm circumference (MAC) 1. With the patient standing (if possible) and at dry weight, measure the circumference of the patient’s right or nonaccess arm using a fiberglass tape. 2. For the maximum accuracy, place the patient’s forearm across the stomach, measure and mark the midpoint between the acromial and olecranon processes. 3. Have the patient relax the arm at his or her side and measure the arm circumference at the mark without compressing the soft tissue. Record to the nearest 0.1 cm. Step II Triceps skinfold (TSF) 1. With the patient’s arm relaxed at his or her side, pick up or lightly pinch a lengthwise double fold of skin with a thumb and forefinger just above the marked midpoint. Have the patient open and close the fist to ensure that none of the muscle is included in the pinch. Note: It may be easiest to start the pinch below the midpoint and work the fingers up to the mark. 2. Hold the calipers parallel to the floor, place them over the fat fold at the mark, to a depth approximately equal to the width of the fat fold. Release calipers while holding the pinch, and take the reading within 3 seconds. Repeat three (3) times and record the average. Step III Mid-arm muscle circumference (MAMC) Calculate as follows: MAMC = MAC - (TSF X 0.314) Step IV Mid-upper arm muscle area (MAMA) 2 Calculate as follows: MAMA = (MAMC) /12.56 Step V Evaluation 1. Compare values to reference standards and record the percent of standard. (Pages 1-28 to 1-32) 2. Use the patient as his or her own standard in subsequent measurements. Note: Measurements on a significant MD population showed few differences from the HANES II norms. Reference: Nelson E: Anthropometry in the Nutritional Assessment of Adults with ESRD. J Ren Nutr 1:162-172, 1991 1-27

REFERENCE VALUES FOR THE TRICEPS SKINFOLD THICKNESS (mm) – Male Age Group Years 15-15.9 16-16.9 17-17.9 18-24.9 25-29.9 30-34.9 35-39.9 40-44.9 45-49.9 50-54.9 55-59.9 60-64.9 65-69.9 70 -70.9

5 5.0 4.0 4.0 4.0 4.0 4.5 4.5 5.0 5.0 5.0 5.0 5.0 4.5 4.5

10 5.0 4.0 4.0 4.0 4.0 4.5 4.5 5.0 5.0 5.0 5.0 5.0 4.5 4.5

15 5.0 5.1 5.0 5.5 6.0 6.5 7.0 6.9 7.0 7.0 6.5 7.0 6.5 6.5

25 6.0 6.0 6.0 6.5 7.0 8.0 8.5 8.0 8.0 8.0 8.0 8.0 8.0 8.0

Percentile 50 75 7.5 11.0 8.0 12.0 7.0 11.0 10.0 14.5 11.0 15.5 12.0 16.5 12.0 16.0 12.0 16.0 12.0 16.0 11.5 15.0 11.5 15.0 11.5 15.5 11.0 15.0 11.0 15.0

85 15.0 14.0 13.5 17.5 19.0 20.0 18.5 19.0 19.0 18.5 18.0 18.5 18.0 17.0

90 18.0 17.0 16.0 20.0 21.5 22.0 20.5 21.5 21.0 20.8 20.5 20.5 20.0 19.0

95 23.5 23.0 19.5 23.5 25.0 25.0 24.5 26.0 25.0 25.0 25.0 24.0 23.5 23.0

Adapted: Frisancho AR: Anthropometric Standards for the Assessment of Growth and Nutritional Status. The University of Michigan Press, 1993

1-28

REFERENCE VALUES FOR THE TRICEPS SKINFOLD THICKNESS (mm) – Female Age Group Years 15.0-15.9 16.0-16.9 17.0-17.9 18.0-24.9 25.0-29.9 30.0-34.9 35.0-39.9 40.0-44.9 45.0-49.9 50.0-54.9 55.0-59.9 60.0-64.9 65.0-69.9 70.0-74.9 Adapted:

5 8.0 10.5 9.0 9.0 10.0 10.5 11.0 12.0 12.0 12.0 12.0 12.5 12.0 11.0

10 9.5 11.5 10.0 11.0 12.0 13.0 13.0 14.0 14.5 15.0 15.0 16.0 14.5 13.5

15 10.5 12.0 12.0 12.0 13.0 15.0 15.5 16.0 16.5 17.5 17.0 17.5 16.0 15.5

25 12.0 14.0 13.0 14.0 15.0 17.0 18.0 19.0 19.5 20.5 20.5 20.5 19.0 18.0

Percentile 50 16.5 18.0 18.0 18.5 20.0 22.5 23.5 24.5 25.5 25.5 26.0 26.0 25.0 24.0

75 20.5 23.0 24.0 24.5 26.5 29.5 30.0 30.5 32.0 32.0 32.0 32.0 30.0 29.5

85 23.0 26.0 26.5 28.5 31.0 33.0 35.0 35.0 35.5 36.0 36.0 35.5 33.5 32.0

90 26.0 29.0 29.0 31.0 34.0 35.5 37.0 37.0 38.0 38.5 39.0 38.0 36.0 35.0

95 32.5 32.5 34.5 36.0 38.0 41.5 41.0 41.0 42.5 42.0 42.5 42.5 40.0 38.5

Frisancho AR: Anthropometric Standards for the Assessment of Growth and Nutritional Status. The University of Michigan Press, 1993

1-29

REFERENCE VALUES FOR MID-ARM MUSCLE CIRCUMFERENCE (cm) Age Group Years 18-24 M 25-34 A 35-44 L 45-54 E 55-64 65-74 F 18-24 E 25-34 M 35-44 A 45-54 L 55-64 E 65-74

5 23.5 24.2 25 24.0 22.8 22.5 17.7 18.3 18.3 18.8 18.6 18.6

10 24.4 25.3 25.6 24.9 24.4 23.7 18.5 18.9 19.2 19.5 19.5 19.5

Percentile 25 50 75 25.8 27.2 28.9 26.5 28.0 30.0 27.1 28.7 30.3 26.5 28.1 29.8 26.2 27.9 29.6 25.3 26.9 28.5 19.4 20.6 22.1 20.0 21.4 22.9 20.6 22.0 24.0 20.7 22.2 24.3 20.8 22.6 24.4 20.8 22.5 24.4

90 30.8 31.7 32.1 31.5 31.0 29.9 23.6 24.9 26.1 26.6 26.3 26.5

95 32.3 32.9 33.0 32.6 31.8 30.7 24.9 26.6 27.4 27.8 28.1 28.1

Reference: Bishop CW, et al: Norms for Nutritional Assessment of American Adults by Upper Arm Anthropometry. Am J of Clin Nutr 34:347, 1982

1-30

REFERENCE VALUES FOR MID-UPPER ARM MUSCLE AREA (cm) – Male Age Group Years 15.0-15.9 16.0-16.9 17.0-179 18.0-24.9 25.0-29.9 30.0-34.9 35.0-39.9 40.0-44.9 45.0-49.9 50.0-54.9 55.0-59.9 60.0-64.9 65.0-69.9 70.0-74.9

5 31.9 37.0 39.6 34.2 36.6 37.9 38.5 38.4 37.7 36.0 36.5 34.5 31.4 29.7

10 34.9 40.9 42.6 37.3 39.9 40.9 42.6 42.1 41.3 40.0 40.8 38.7 35.8 33.8

15 36.9 42.4 44.8 39.6 42.4 43.4 44.6 45.1 43.7 42.7 42.7 41.2 38.4 36.1

25 40.3 45.9 48.0 42.7 46.0 47.3 47.9 48.7 47.9 46.6 46.7 44.9 42.3 40.2

Percentile 50 75 46.3 53.1 51.9 57.8 53.4 60.4 49.4 57.1 53.0 61.4 54.4 63.2 55.3 64.0 56.0 64.0 55.2 63.3 54.0 62.7 54.3 61.9 52.1 60.0 49.1 57.3 47.0 54.6

85 56.3 63.6 64.3 61.8 66.1 67.6 69.1 68.5 68.4 67.0 66.4 64.8 61.2 59.1

90 65.7 66.2 67.9 65.0 68.9 70.8 72.7 71.6 72.2 70.4 69.6 67.5 64.3 62.1

95 63.0 70.5 73.1 72.0 74.5 76.1 77.6 77.0 76.2 77.4 75.1 71.6 69.4 67.3

Adapted: Frisancho AR: Anthropometric Standards for the Assessment of Growth and Nutritional Status. The University of Michigan Press, 1993

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REFERENCE VALUES FOR MID-UPPER ARM MUSCLE AREA (cm) – Female Age Group Years 15.0-15.9 16.0-16.9 17.0-17.9 18.0-24.9 25.0-29.9 30.0-34.9 35.0-39.9 40.0-44.9 45.0-49.9 50.0-54.9 55.0-59.9 60.0-64.9 65.0-69.9 70.0-74.9

5 24.4 25.2 25.9 19.5 20.5 21.1 21.1 21.3 21.6 22.2 22.8 22.4 21.9 22.2

10 25.8 26.8 27.5 21.5 21.9 23.0 23.4 23.4 23.1 24.6 24.8 24.5 24.5 24.4

15 27.5 28.2 28.9 22.8 23.1 24.2 24.7 25.5 24.8 25.7 26.5 26.3 26.2 26.0

Percentile 25 50 29.2 33.0 30.0 33.6 30.7 34.3 24.5 28.3 25.2 29.4 26.3 30.9 27.3 31.8 27.5 32.3 27.4 32.5 28.3 33.4 28.7 34.7 29.2 34.5 28.9 36.6 28.8 34.3

75 37.3 38.0 39.6 33.1 34.9 36.8 38.7 39.8 39.5 40.4 42.3 41.1 41.6 41.8

85 40.2 40.2 43.4 36.4 38.5 41.2 43.1 45.8 44.7 46.1 47.3 45.6 46.3 46.4

90 41.7 43.7 46.2 39.0 41.9 44.7 46.1 49.5 48.4 49.6 52.1 49.1 49.6 49.2

95 45.9 48.2 50.8 44.2 47.8 51.3 54.2 55.8 56.1 55.6 58.8 55.1 56.5 54.6

Adapted: Frisancho AR: Anthropometric Standards for the Assessment of Growth and Nutritional Status. The University of Michigan Press, 1993

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OTHER MEASURES OF BODY COMPOSITION Assessment of:

Advantages

Limitations

Dual Energy X-Ray Absorptiometry (DEXA) (K/DOQI) Hydrodensitometry (Underwater Weighing)

Methods

Bone/bone mineral content, fat mass, & lean body mass

Validated high precision/pt acceptance, low radiation, can provide localized body comp, suitable for all ages Most accurate in CKD if combined with DEXA and volume of TBW.

Bioelectric Impedance (BIA)

Total body water, lean body mass, fat-mass

Easy to perform, small time investment, high patient acceptance, little training needed, portable

Creatinine Kinetics

Lean body mass

Near Infrared Interactance

Body composition, % body fat

Relatively easy, similar to other procedures such as UKM Not influenced by state of hydration, consistent measurements, ease of use

Affected by hydration, tissue density, assumption re soft tissue content near bone, Cost, inconvenience Difficult for patient (submersion/exhaling air from lungs), special equipment needed May not distinguish between changes in LBM versus hydration status. May be more useful in populations rather than individuals Limited research, need to collect urine/dialysate

Lean body mass

Limited research in dialysis patients

References: DeVita MV, Stall S: Dual-Energy X-Ray Absorptiometry: A Review. J Ren Nutr 9(4):178-181, 1999 Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997 Stall S, et al: BIA and DEXA to Monitor Nutritional Status. PD Int 15(Suppl):S59-62, 1995 NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000. 1-33

SUBJECTIVE GLOBAL ASSESSMENT (SGA) SGA is the overall evaluation by an experienced clinician of the history and physical exam to rate patients as well nourished, mild to moderately malnourished, or severely malnourished. The focus of SGA is nutrient intake and body composition. Both the K/DOQI practice guideline for peritoneal dialysis adequacy and nutrition recommend SGA as a valid and clinically useful measure of protein-energy status in maintenance dialysis patients. The recommended SGA uses a 7 point scale (in place of the A-B-C, ratings used in the traditional SGA) with 1-2 ratings for severe malnutrition, 3-4-5 ratings for moderate to mild malnutrition, and 6-7 ratings for well nourished. It uses only four of the main categories from the traditional SGA: weight change, dietary intake and GI symptoms (anorexia, nausea, vomiting, and diarrhea), loss of subcutaneous fat, and loss of muscle tissue. The traditional SGA is reviewed here and the K/DOQIspecific categories are indicated by italics. SGA is meant to be subjective, based on the clinician’s expertise and experience. Thus, the ratings that follow are only suggestions. Training and agreement among team members will minimize interrater variability. A one-page rating form can be used to record observations and the overall rating. The final rating is not an average of the individual category ratings, but a subjective assessment by the clinician. A number of rating forms have been published for use or adaptation: Baxter Healthcare-Renal Division, McGaw Park, IL Detsky AS: J Parenter Enteral Nutr 11:440-446, 1987 McCann L: Dialysis and Transplantation 25(4):190, 1996 Page C: Nutritional Assessment and Support- A Primer, Williams & Wilkins, Baltimore, 1994 NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000.

1-34

Editor’s Note: The use of SGA in the chronic kidney disease population creates the challenge of maintaining the subjectivity of the tool while trying to maximize interrater consistency. Objective measures of nutrition status are critical to the assessment of CKD patients, but are only a part of the entire picture. Therefore, we must preserve the intangible value of a clinician’s judgement. Many professionals have difficulty embracing the SGA tool because it seems too simple. However, SGA has demonstrated its value as a stand-alone assessment technique, used in conjunction with, rather than combined with, other objective measures. (CAN-USA) There is also discussion regarding the use of the traditional A-B-C ratings versus the 7 point scale (CAN-USA and K/DOQI). The 7 point scale allows the clinician to more accurately quantify the status of the patient. Assigning a B rating does not provide the same level of sensitivity as assigning a rating of 3, (the most negatively significant level of malnutrition in the mild to moderate category) or a 5 (the least negatively significant level of malnutrition in the mild to moderate category). In addition, the endorsement of the 7 point scale within the K/DOQI Guidelines for Nutrition in CRF, provides an opportunity to standardize practice. Standardization of practice allows us to compare populations, to test the long-term validity of the tool in CKD patients, to observe outcomes of nutrition recommendations, and develop universal clinical performance measures. While clinical expertise and experience is the most important aspect of SGA, the following tips have been developed from performing SGA in varying populations around the world. They are put forth for your consideration: 1. 2. 3. 4. 5. 6. 7.

Training and a review of technique with colleagues who will be assessing common patients is invaluable. Dietary intake can be the most important early indicator of nutritional risk. Thus, an estimate of current intake compared to recommended nutrient levels (considering the duration of deficit or excess) is a worthwhile part of SGA. Patterns of muscle wasting or preservation may be inconsistent depending on the physical activity/abilities of the patient. Patient perspective and insight can be helpful in all aspects of SGA. Tissue loss should be evaluated in relation to weight changes, especially in the baseline assessment. Elderly patients typically have age-related tissue losses that mimic malnutrition. Get the patient’s perspective. With advance planning and instruction, it is possible to observe most or all of the muscle/fat sites toward the end of dialysis (at or close to dry weight) treatment without compromising the patient’s privacy. Use universal precautions. A majority of patients are able to complete a simple questionnaire to provide some of the information needed for SGA. 1-35

SGA WEIGHT/MEDICAL/NUTRITION HISTORY Use of standard questions can help improve the accuracy and consistency of SGA ratings. The following questions may help you gather the information you need for the medical history portion of SGA. Some or most of this information could also be obtained using a simple, patient-completed questionnaire. Usual adult weight? Current weight? Weight six months ago? Weight 2 weeks ago? Any signs of fluid overload? Edema? SOB? High B/P? Current appetite/intake? Is intake adequate to meet needs and recommendations? Change in previous six months? Change in past two weeks? GI Distress? Anorexia—frequency/duration of anorexia? Nausea—frequency/duration of nausea? Vomiting—frequency/duration of vomiting? Diarrhea—frequency/duration of diarrhea? Changes in function or activity related to malnutrition (Activities of daily living, gardening, volunteer work, household chores, energy levels, etc.)? Significant metabolic stress other than CKD? (Fever-degrees above normal and duration; use of steroids-dose dependent, significant infection, etc.) 1-36

SCHEMATIC OF MUSCLE TO GUIDE ASSESSMENT OF WASTING (Fat store sites are in italics).

1-37

SGA Part I - Review medical record/use specific, detailed questions to assess current status. (K/DOQI in italics) Weight 1. Weight change over 6 months (Use rating as listed even in obese patient) a. <5% = A rating (6 or 7) b. 5-10% = B rating (3 or 4 or 5) c. >10% and sustained loss = C rating (1 or 2) d. 10% but recovery to 5-10% = B rating (3 or 4 or 5) e. Sustained improvement = one level up from previous 2. Weight change over previous two weeks a. No change, normal weight = A rating (6 or 7) b. Increasing or increased = rate one level up from previous rating c. Decreasing = rate one level below previous rating Dietary Intake 1. Change in intake (duration and degree) 2. Base ratings on current and prior status: a. Intake adequate for needs, no change or change is slight/short duration = A (6 or 7) b. Borderline, decreasing = B (3 or 4 or 5) c. Unable to eat, starvation = C (1 or 2) GI Symptoms 1. Nausea, vomiting, diarrhea, anorexia 2. Duration and frequency a. Symptoms > 2 weeks, almost daily = C (1 or 2) b. Minor or no symptoms, occasional = A (6 or 7) c. Degree and frequency of symptoms between A and C = B (3 or 4 or 5)

1-38

Functional Status 1. Decreased strength or stamina due to malnutrition (See page 1-42 for examples) 2. Duration and degree of dysfunction (rate in relation to normal or previous SGA rating) Metabolic Stress/Disease State/Co-morbidities 1. Low-moderate (infection, skeletal trauma, malignancy) 2. High stress (ulcerative colitis with diarrhea) Part II Physical Exam (Use universal precautions/protective hand washing) Exam areas: Subcutaneous Fat Below the eye

Triceps/Biceps

Tips

View patient straight on, touch above cheek bone with permission Arm bent, roll skin between fingers, do not include muscle in the pinch

Severe Malnutrition 1 or 2 (C)

Mild-Moderate Malnutrition 3 or 4 or 5 (B)

Well Nourished 6 or 7 (A)

Hollow look, depressions, dark circles, loose skin

Slightly dark circles, somewhat hollow look

Slightly bulged fat pads. Fluid may mask loss

Very little space between folds fingers touch

Some depth to pinch, but not ample

Ample fat tissue obvious between folds of skin

1-39

Muscle Wasting Temple

Clavicle

Shoulder

Tips Observe straight on, have pt turn head side to side Look for prominent bone. Make sure pt is not hunched forward Arms at side, look at shape

Scapula

Have patient extend hands straight out, push against solid object

Interosseous Muscle

Thumb side of hand; pads of thumb/ forefinger touching

Severe Malnutrition Hollowing, scooping, depression Protruding, prominent bone Shoulder to arm joint looks square Prominent, visible bones, depressions between ribs/scapula or shoulder/spine Depressed area between thumbforefinger

Mild-Moderate Malnutrition Slight depression

Well Nourished Can see/feel welldefined muscle

Visible in male, some protrusion in female Acromion process may protrude slightly Mild depression, or bone may show slightly

Not visible in male, visible but not prominent in female Rounded, curves at arm/shoulder/neck

Slightly depressed

Muscle bulges, could be flat in wellnourished person

Bones not prominent, no significant depressions

1-40

Muscle Wasting

Tips

Severe Mild-Moderate Well Nourished Malnutrition Malnutrition Knee (Lower body Have patient sit Bones prominent, Knee cap less Muscle protrudes is less sensitive to with leg propped little sign of muscle prominent, more bones not change) up, bent at knee around knee cap rounded prominent Quadriceps Not as sensitive as Depression/line on Mild depression on Well rounded, upper body thigh, obviously inner thigh developed thin Calf Observe side and Thin, minimal or Not well developed Well-developed front view no muscle bulb of muscle definition Edema - in dialysis, edema is important for quantifying weight loss in view of fluctuating fluid balance. R/O other causes of edema, patient at dry weight

View sacrum in activity-restricted patient; ankle in mobile patient

Significant swelling

Mild to moderate swelling

No sign of fluid accumulation

Reference: McCann L: Subjective Global Assessment as it pertains to the nutritional status of dialysis patients. Dialysis & Transplantation, 25(4):190, 1996

1-41

CRITERIA FOR ESTIMATION OF PERFORMANCE OR FUNCTIONAL STATUS The scale below is a guide to the assessment of a patient’s functional status. During SGA, look for changes that are related to malnutrition (difficulty with ambulation secondary to muscle wasting). In the general assessment of renal patients, look for changes that are related to chronic disease and nutrition. In CKD, compare functional status prior to kidney disease/dialysis in initial assessment or at last SGA to their current functional status. Grade 0 1

2

3 4

Scale Fully active, able to carry on all predisease performance without restriction. Fully capable of hard work. (Karnofsky 90-100) Restricted in physically strenuous activity, but ambulatory and able to carry out light or sedentary type activities (office). (Karnofsky 70-80) Ambulatory and capable of all self-care, but unable to work. Up and about >50% of waking hours. (Karnofsky 50-60) Capable of only limited self care, confined to bed or chair more than 50% of waking hours. (Karnofsky 30-40) Completely disabled, confined to bed or chair, no self care. (Karnofsky 10-20)

Possible SGA Score 7 6-5

4-3

2 1

Reference: Stanley KE: Prognosis Factors for survival in patients with inoperable lung cancer. J Natl Cancer Inst. 65:25-29, 1980

1-42

DIETETIC-SPECIFIC NUTRITIONAL DIAGNOSTIC CODES (D-S NDCs) Category/Code Absence of/Limited D1.000

Description Nutrition Service/Prof. Nutritionist Contact Nutritional Collateral Systems

NDC # D1.001 D1.002

Altered/ Alteration In D2.000

Body Composition Integrity Bowel Elimination Drug Deposition Metabolism Nutrient Deposition Nutritional Biochemistry Integrity Feeding and Treatment/Diagnostic Schedules

D2.001 D2.002 D2.003 D2.004 D2.005 D2.006 D3.001

Nutrition Education Nutrition Knowledge Home Enteral/Parenteral Product Assistance Home Food Service Assistance Home Therapeutic Diet/Product Assistance

D4.001 D4.002 D5.001 D5.002 D5.003

Conflict In D3.000 Deficit In D4.000 Dependent On D5.000

1-43

DIETETIC-SPECIFIC NUTRITIONAL DIAGNOSTIC CODES (D-S NDCs) (Cont.) Category/Code Excessive D6.000

Imbalance D7.000

Impaired D8.000

Inactive Role In D9.000

Description Calorie Allowance/Intake Fiber Allowance/Intake Protein Allowance/Intake Vitamin/Mineral Allowance/Intake Water/Fluid Allowance/Intake Electrolyte Energy Nutrient Water/Fluid Activity Performance Cognition and Behavior Fecundity/Fertility Growth/Development/Function Home Maintenance of Dietary Needs Lactation Performance Social Performance Work Performance Maintaining Adequate Nutrition

NDC # D6.001 D6.002 D6.003 D6.004 D6.005 D7.001 D7.002 D7.003 D7.004 D8.001 D8.002 D8.003 D8.004 D8.005 D8.006 D8.007 D8.008 D9.001

1-44

DIETETIC-SPECIFIC NUTRITIONAL DIAGNOSTIC CODES (D-S NDCs) (Cont.) Category/Code Inadequacy D10.000

Inappropriate D11.000

Intolerance D12.000

Description Calorie Allowance/Intake Carbohydrate Fat-Essential Fatty Acids Feeding Route Fiber Allowance/Intake Food-Diet Consistency Mineral Protein-Amino Acid Allowance/Intake Vitamin Water, Fluids/Fluid Balance Treatment Time Caloric Distribution Dietary Habits Feeding Route Food Role Perception/Food Abuse Protein Distribution Drug/Chemical Substance in Food Food(s)/Nutrient(s)

NDC # D10.001 D10.002 D10.003 D10.004 D10.005 D10.006 D10.007 D10.008 D10.009 D10.010 D10.011 D11.001 D11.002 D11.003 D11.004 D11.005 D12.001 D12.002

1-45

DIETETIC-SPECIFIC NUTRITIONAL DIAGNOSTIC CODES (D-S NDCs) (Cont.) Category/Code Misinformation D13.000 Misuse D14.000

Nonacceptance D15.000 Noncompliance D16.000 Possibility of/Possibility of Developing D17.000 Potential Consequences of D18.000

Description Nutrition

NDC # D13.001

Enteral Product Nutrient Supplement Other Food Substance Parenteral Product Therapeutic Diet/Product Food Item(s)/Nutritional Products

D14.001 D14.002 D14.003 D14.004 D14.005 D15.001

Nutritional

D16.001

A Specific Disease Morbidity, Incr. Duration/Severity of Illness Mortality, Increased Risk of Altered Nutrient Function(s)

D17.001 D17.002 D17.003 D18.001

1-46

DIETETIC-SPECIFIC NUTRITIONAL DIAGNOSTIC CODES (D-S NDCs) (Cont.) Category/Code Prevention, Decreasing, Eliminating Need for/ Use of D19.000 Self Assessment Risk Factors D20.000 Suboptimal D21.000 Toxicity D22.000 Undesirable D23.000

Unwellness D24.000

Drug Therapy

Description

NDC # D19.001

Nutritional

D20.001

Pregnancy Outcome Nutritional Resiliency Nutrient Food/Diag/Tx Schedule Interaction Med/Food/Nutrient Interaction Metabolic Setpoint Overweight Status Underweight Status Weight (e.g. loss/gain) Nutritional

D21.001 D21.002 D22.001 D23.001 D23.002 D23.003 D23.004 D23.005 D23.006 D24.001

Reference: (Used with permission) © M.A. Kight and Biodietetic Associates, 1994

1-47

MEDICAL NUTRITION THERAPY (MNT) Medicare Part B Coverage: Provides for payment of nutrition services for certain beneficiaries who have diabetes or kidney disease. Kidney disease is defined as chronic renal insufficiency and post-transplant care provided up to 36 months after transplant. The IOM defines chronic renal insufficiency as the stage of renal disease associated with a reduction of renal function not severe enough to require dialysis or transplantation (GFR 13-15 mL/min/1.73m2). Diabetes mellitus (DM) Type 1 is defined as an autoimmune disease that destroys the beta cells of the pancreas leading to insulin deficiency. DM Type 2 is defined as familial hyperglycemia that occurs primarily in adults...caused by an insulin resistance where etiology is multiple and not well understood. Institute of Medicine (IOM) lists the diagnostic criterion for diabetes as a fasting glucose tolerance test >126 mg/dL. Current Procedural Terminology (CPT) Codes: 97802 - Medical nutrition therapy; initial assessment and intervention, individual, face-to-face with the patient, billed in 15 minute intervals 97803 - Reassessment and intervention, individual, face to face with the patient, billed in 15 minute intervals 97804 - Group (2 or more individuals), billed in 30 minute intervals Fees: Medicare MNT payment is based on the geographical area in which services are provided. (Medicare MNT Payment Schedule 2002 by Geographic Area) References: American Dietetic Association at http://www.eatright.org Centers for Medicare and Medicaid Services at http://hcfa.gov/stats/cpt/rvudown.htm 1-48

COMMON PHYSICAL SIGNS OF MALNUTRITION Protective hand washing and other protective precautions, appropriate to the situation, should be taken prior to any physical contact with patients. (Standard precautions) Body Part Hair

Face

Eyes

Signs Lack of luster Thin and sparse Dyspigmentation Easy pluckability Diffuse depigmentation Nasolabial dyssebacia

Conjunctival xerosis Bitot’s spots Corneal xerosis

Tongue

Keratomalacia Atrophic papillae

Description

Nutrient

Changes not related to salt water/sun/heat/physical damage, cosmetic treatment, or scalp disease Occurs in dark skinned individuals Yellow, greasy appearance from plugged ducts of sebaceous glands around nose/lips Dryness, thickening of bulbar conjunctiva of exposed eye White-grey foamy plaque usually laterally to cornea Hazy/opaque appearance of cornea Softening of cornea Smooth, slick appearance

Protein Protein/Biotin/Zinc Protein Protein/Zinc/EFA Protein/calorie B-Complex

Vitamin A Vitamin A Vitamin A Vitamin A Iron 1-49

COMMON PHYSICAL SIGNS OF MALNUTRITON (Cont.) Body Part Lips/ Mucous Membrane Gums

Skin

Nails

Musculoskeletal

Signs

Description

Nutrient

Angular Stomatitis Cheilosis Pallor

Fissuring at angles of mouth Red, swollen ulceration of lips

Riboflavin B Complex Iron

Spongy, Bleeding Bright red Ulceration Xerosis Follicular Hyperkeratosis Petechiae Pellagrous Dermatosis Flaky Paint Dermatosis Koilonychia Splinter hemorrhages White spotting Epiphyseal Enlargement Beading of Ribs

Swollen gingival tissue Red discoloration of gingiva Inflammation (ulceration/stomatitis) Dryness/scaling Hypertrophy of skin around hair follicles with formation of plaque Hemorrhagic spots in skin/mucosa Skin hyperpigmentation Scaling skin, leaves hypo-pigmented spots Spoon shaped deformity of nail Semi-circular lattice in nail beds Spots/dashes on nail Enlarged ends of long bones Enlarged cartilage at rib junctions

Vitamin C Vitamin A Vit. C, Folate, B12 Essential FA/Zinc Vitamin A Vitamin C, K Niacin Protein Iron Vitamin C Zinc Vitamin C, D Vitamin D

References: Kight MA: Physical Assessment in Renal Disease. CRN Quarterly 11:9-12, 1987 McLaren DS: A Colour Atlas and Text of Diet-Related Disorders, Mosby-Year Book Europe, 1992 Simko M, et al: Nutrition Assessment: A Comprehensive Guide for Planning Intervention, ASPEN, 1995 1-50

Chapter 10: ADEQUACY OF DIALYSIS AND UREA KINETIC MODELING

GENERAL INFORMATION The goals of this chapter are to give some simple insight into the components of kinetic modeling, to guide the clinician in interpreting the Kt/V, and to review the adequacy guidelines that were formulated by K/DOQI. While some simple formulas are given, it is recognized that access to computer software, on-line, or calculator kinetic modeling programs is widespread and few people calculate Kt/V, protein equivalent of nitrogen appearance (PNA) by hand. Regardless of how adequacy is measured, targets below should be interpreted in conjunction with other clinical parameters relating to the individual patient.

K/DOQI SUGGESTED ADEQUACY TARGETS, 2001 Modality

Kt/V

CAPD H/HA L/LA* NIPD CCPD HEMODIALYSIS

2.0 2.0 2.2 2.1 (spvv model) Rx ≥ 1.3 Del ≥ 1.2 URR ≥ 65%

CrCl/L/1.73 2 m 60 L/wk 50 L/wk 66 63 NA

Frequency of Adequacy Testing PET, Kt/V, CrCl, urine at month 1; Kt/V, CrCl, urine at months 4 & 6; then: Kt/V, CrCl, urine ≥ every 4 months Include SGA and PNA calculations If there is a discordance in the parameters, use the Kt/V Formal spvv urea kinetic modeling is recommended at least monthly. Substitute natural log formula Kt/V or URR, if formal urea kinetic modeling cannot be performed Other recommendations: Use specific, consistent blood sampling techniques (pg 10-7) and adequacy testing methods; provide routine error analysis and prompt intervention as needed to meet adequacy and nPCR targets

*Membrane transport characteristic: H=high, HA=high average, L=low, LA=low average Low and low average transporters have better survival and technique survival, but without residual urine output may not be able to achieve a CrCl of 60 L/wk, even when Kt/V is adequate. Thus the CrCl target can be set slightly lower as long as patients are observed closely for evidence of inadequate dialysis. 10-2

KINETIC MODELING GLOSSARY Access Recirculation - when the blood flow rate set by the blood pump is higher than the access blood flow, some outflow blood will recirculate within the access back into the inflow stream. This mixes fresh blood from the arterial segment and dialyzed blood from the venous segment. Actual Weight - current body weight expressed in kilograms. Body Surface Area - total surface area of the body, expressed in square meters/derived from height and weight. Cardiopulmonary Recirculation - dialyzed blood from the venous outflow of the blood access is recirculated back into the arterial inflow of the blood access through a circulation loop that includes central veins, right heart, lungs, and the left heart reducing effective blood clearance. Clearance (K) - dialyzer urea clearance, expressed as plasma water clearance in ml/min or L/min or the volume of solution that is cleared or depleted of a solute during a given period of time. It can also mean the rate of mass transport per unit of concentration gradient. The K in formal urea kinetic modeling includes all clearance including urinary. Compartmental Disequilibrium - spvv kinetic model assumes solute is distributed in a single, well mixed, homogenous body and is uniformly removed from the total volume. In reality, solute is removed from the peripheral compartment and the central compartment lags behind at a higher concentration of solute. At the start of dialysis both compartments are in equilibrium, but at the end of dialysis, disequilibrium causes a rebound of the solute concentration into the peripheral compartment after the treatment. Depner T. Sem Dial 5(2):147-154, 1992 Desirable Body Weight - same as ideal body weight. Direct Dialysis Quantification - direct measurements total effluent dialysate urea or in aliquots of dialysate; may represent a gold standard for assessing urea removal, but is laborious. Several measurements of dialysate must be taken to prevent magnification of small errors when results are multiplied by the total effluent dialysate. dpvv Kt/V = double pool, variable volume Kt/V. Dry Weight = post dialysis weight at which most or all of the excess body fluid has been removed Equilibrated Kt/V (eKt/V) = delivered dialysis dose obtained by processing a single pool Kt/V through a formula to estimate the equilibrated (double pool) Kt/V, or Kt/V calculated with a 30 minute postBUN. 10-3

KINETIC MODELING GLOSSARY (Cont.) eKdrt/V - total equilibrated Kt/V including urea clearance from both dialysis and residual urine output. eKdt/V - equilibrated Kt/V from the clearance of urea by dialysis alone. This allows the clinician to observe what portion of the eKt/V results from the residual urine output. K - dialyzer urea clearance, expressed as plasma water clearance in ml/min or L/min. Kdrt/V - total Kt/V that includes clearance from dialysis and residual urine output or KrU. Kdt/V - Kt/V that includes dialysis clearance only. Allows clinician to observe the prescribed Kt/V for a specific prescription if the patient’s residual urine output decreases to zero. Kinetic Volume - determined from the drop in BUN during a single dialysis treatment (can also be called “Current Volume”). A deviation in kinetic or current volume in a single patient serves as a flag for errors in delivery of dialysis. Kinetic volume, in a problem free dialysis treatment, should approximate the volume from surface area (VSA). KoA - overall dialyzer permeability for urea, ml/min (product of the membrane permeability/surface area). Kt/V - dose of dialysis treatment as determined by the solute clearance-time product normalized to the individual’s volume of urea distribution or urea clearance (K ml/min or L/min) times the treatment length (T minutes) divided by urea distribution volume (V) is the total urea clearance provided by the dialyzer and any residual urine output. Normal Body Weight - median weight of healthy Americans, same age range/height/gender/frame size. Normalized Protein Catabolic Rate (nPCR) - protein catabolic rate in gm/day normalized as some function of weight (Recommended: nPCR = PCR/ (V/0.58) to provide gm/kg/day). (More correct terminology is nPNA as below). Normalized Protein Equivalent of Total Nitrogen (nPNA) - PNA normalized to a function of weight (as above). Protein Catabolic Rate (PCR) - amount of protein catabolized in grams/d. (More correct terminology is PNA as below). Protein Equivalent of Total Nitrogen Appearance (PNA) - expresses total nitrogen appearance in terms of protein in grams per day (normalized is grams per kilogram per day). The conversion is based on the fact that the nitrogen content of mixed proteins is approximately 16% and quantitatively, most of the nitrogenous compounds lost from the body are either metabolites of protein (urea) or actual proteins and peptides (in peritoneal dialysate). See formulas page 10-11 and 10-23 to 10-24. 10-4

KINETIC MODELING GLOSSARY (Cont.) Relative Body Weight - dry body weight expressed as a percentage of the normal body weight for an individual of the same gender, height, and frame size. More commonly known as SBW. Residual Renal Function (RRF) - remaining kidney function in a patient receiving dialysis or in advanced CKD; GFR expressed in milliliters per minute or liters per day. (Terminology in this chapter has been changed to residual urine output). Standard Body Weight = Weight for like individual (gender, frame size, height, age) as determined by NHANES II. spvv Kt/V = single pool, variable volume Kt/V. T - dialysis treatment time. (In Kt/V the t also includes frequency of dialysis). Total Body Water (TBW) - estimated volume of distribution of solute expressed in liters. Total Nitrogen Appearance (TNA) - the sum of all outputs of nitrogen from the body including dialysate/feces/urine plus the change in body nitrogen, expressed in grams of nitrogen per day. Urea Nitrogen Appearance - net appearance of urea nitrogen in body fluids/outputs (urine, dialysate, fistula drainage). Urea Reduction Ratio (URR) - adequacy measure based on the change in BUN for a single dialysis treatment; does not account for any urinary clearance of urea, the individual patient volume, ultrafiltration rate, or rebound, thus cannot be strictly correlated with Kt/V. Has been shown to be significant predictor of mortality in HD patients. V - urea distribution volume or total body water. Volume From Surface Area (VSA) - is calculated using a formula (see page 10-9). The VSA is fairly stable unless there is a significant change in weight such as with acute illness or amputation. VSA may be slightly different from kinetic volume in the first few modeling sessions if the patient is very lean, very obese or has excessive fluid weight. Reference: Kopple JD, et al: Proposed Glossary for Dialysis Kinetics. Am J Kidney Dis 26(6):963-981, 1995

10-5

METHODS OF MEASURING HEMODIALYSIS ADEQUACY Method

Formal Urea Kinetic Modeling

Kt/V Natural Log Formula

Urea Reduction Ratio (URR)

Advantages

-Can be used to develop a prescription -Provides information to help identify errors in delivery of dialysis -Permits calculation of PNA -Has outcome study to identify targets -Accounts for volume changes (UF/ convective transport) -Correlates with spKt/V -Best alternative after formal UKM -Ease of calculation -Significant predictor of mortality

Kt/V Derived from Percent Reduction of Urea (PRU) Urea Removal/ On-line Monitor

Very promising

Disadvantages

-Complex calculations require computer/calculator -Assumed parameters of clearance/volume -Accurate data is critical (blood draw technique, recording of time, BFR) -Does not support the calculation of PNA (Nomogram is not well tested) -Does not provide analysis/quantitative Rx calculation -Does not provide volume or means of QA -Does not provide analysis/quantitative Rx calculation -Doesn’t support calculation of PNA -Doesn’t consider residual urine output -Much less precise in relation to UKM -Incorrect in ≥ 20% of patients compared to UKM -Not suitable for routine monitoring of delivered dose of dialysis -Lack of clinical experience, patient outcomes, targets -Expense of equipment

Reference: NKF K/DOQI Clinical Practice Guidelines for Hemodialysis Adequacy, Update 2000 Am J Kidney Dis. 37(1) Suppl 1, January, 2001 10-6

PARAMETERS THAT AFFECT ADEQUACY Treatment Blood Flow Rate Dialysate Flow Rate Dialyzer Capabilities Frequency/Duration

Patient Height/Weight/Volume Chemistries/Dietary Intake Residual Urine Output

FORMAL UREA KINETIC MODELING (Kt/V) COMPONENTS

K = Total Clearance Dialyzer efficiency Blood & dialysate flow rates Residual Renal Function

T = Time Frequency Duration

V = Volume Body water in which urea is distributed

Accurate blood sampling techniques and data recording are necessary for accurate UKM results. For spvv formal urea kinetic modeling: PreBUN should be drawn immediately prior to the dialysis treatment, taking care to prevent dilution with saline or heparin. PostBUN should be drawn with the slow flow, stop pump technique which prevents sample dilution with recirculated blood and minimizes confounding effects of urea rebound.

2-7:

10-7

BODY WATER VOLUME 1. Affected by height, weight, age, gender, body fat or muscle stores. 2. Remains relatively constant over time if weight is stable. 3. Can be measured three ways: a. % Body Weight (50 - 60% male, 50 - 55% female). Inaccurate in approximately 20 - 25% of population. b. Surface Area (considers ht, wt, gender). Inaccurate in approximately 15% of population. c. Kinetic or variable volume is determined kinetically from the drop in BUN during a single dialysis treatment; most accurate, but requires computer assistance. Is skewed when there is an error in the delivery of dialysis. 4. Body water may be low in dialysis patients secondary to low muscle mass, thus what is abnormal in a person without kidney disease may be normal for a dialysis patient. Expected values for disease-free individuals: Lean male - 57% Lean female - 52% Obese - 35-40% Very lean - 65% 5. Deviations in kinetic V in a single patient serve as a flag for errors in dialysis clearance. 6. When clearance < expected with a given dialyzer/BFR/DFR/VSA/time/frequency, the kinetic V will be skewed higher than VSA. The model assumes actual body water is > VSA (calculated) because urea clearance was < expected (there was a larger body of water from which urea was being cleared). 7. Conversely, when clearance is > than expected with specific treatment parameters, kinetic V will be lower than VSA. The model assumes that the actual body water is smaller than VSA (calculated) since urea clearance was > expected (there was a smaller body of water from which urea was being cleared).

10-8

VOLUME FROM SURFACE AREA (VSA) CALCULATION FORMULAS Hemodialysis: Recommended VSA Formula BEI Derived Formula:1 Volume (TBW) = -(0.07493713 x age) - (1.01767992 x male) + (0.12703384 x ht) - (0.04012056 x wt) + (0.57894981 x diabetes) - (0.00067247 x wt2) -0.03486146 x (age x male) + 0.11262857 x (male x wt) + 0.00104135 x (age x wt) + 0.0186104 x ( ht x wt) Wt=pt weight/kg Ht=pt height/cm Other factors: Male=1.0 Diabetic=1.0 (if not diabetic/male, values=0) Peritoneal Dialysis: Recommended VSA Formulas Watson: Male: Volume = 2.447-(0.09516 x ageyrs) + (0.1074 x ht cm)+ (0.3362 x wtkg) Female: Volume = -2.097 + (0.1069 x htcm) + (0.2466 x wtkg) Hume & Wyers: (J Clin Path 24:234-238, 1971) Male: Volume = (0.194786 x ht cm) + (0.296785 x wtkg) - 14.012934 Female: Volume = (0.34454 x ht cm) + (0.183809 x wtkg) - 35.270121 Mellits-Cheek Method: Pediatrics Boys: Volume = -1.927 + (0.465 x wtkg) +(0.045 x htcm) when height is ≤ 132.7 cm Volume = -21.993 + (0.406 x wtkg) + (0.209 x htcm) when height is > 132.7 cm Girls: Volume = 0.076 + (0.507 x wtkg) + (0.013 x htcm) when height is ≤ 110.8 cm Volume = -10.313 + (0.252 x wtkg) + (0.154 x htcm) when height is > 110.8 cm Reference: NKF K/DOQI Clinical Practice Guidelines for HD Adequacy, 2000 Update, Am J Kidney Dis. 37(1) Suppl 1, January, 2001 1Chertow GN, et al: Development of a population-specific regression equation to estimate TBW in HD patients. KI 51:1578-1582, 1997 10-9

DIFFERENCES BETWEEN SINGLE POOL AND DOUBLE POOL KINETICS Single Pool* Does not account for different rates of urea transfer between body compartments or different blood flow rates to organs.

Double Pool More accurate in quantifying true intradialytic urea removal and more precise PNA; 30 minute post BUN is not practical for all patients; formula to calculate eKt/V from single pool Kt/V: eKt/V = spKt/V – (0.6)(K/V) +0.03

With increased dialyzer efficiency, urea removal can exceed diffusive transfer rates which creates urea rebound for 3060 minutes after treatment. Blood sampling immediately at the end of treatment does not reflect urea that equilibrates from tissues back into blood, thus BUN is falsely low, and Kt/V is overestimated by about 0.2. Rebound varies from patient to patient. (One study showed a mean rebound of about 17% at 30 minutes after treatment, some patients as high as 45% rebound). Rebound begins within minutes of the end of treatment. Most patients equilibrate within 15 minutes, others take up to 60 minutes. Rebound is exaggerated in small patients, cardiac compromised patients, and treatments complicated by intradialytic hypotension. *K/DOQI Clinical Practice Guidelines for HD Adequacy recommend the use of single pool variable volume kinetic modeling because outcome studies are lacking for double pool kinetic modeling. References: Daugirdas JT, Ing TS: Handbook of Dialysis, 2nd Edition, Little, Brown, & Co., 1994 NKF K/DOQI Clinical Practice Guidelines for HD Adequacy, 2000 Update, Am J Kidney Dis. 37(1) Suppl 1, Jan, 2001

10-10

HEMODIALYSIS FORMULAS FOR UREA KINETIC MODELING (UKM) 1. Measure recirculation using a nonurea-based dilutional or two needle urea-based method. Any recirculation is abnormal, but recirculation of >10% in the two needle method or >5% with nonurea-based dilutional method should be investigated. Check needle placement prior to further studies when recirculation exceeds 20%. Perform the test after approximately 30 minutes of treatment with ultrafiltration turned off. a. Draw arterial (A) and venous (V) line samples. Immediately reduce blood flow rate (BFR) to 120 mL/minute. b. Turn blood pump off exactly 10 seconds after reducing BFR. Clamp arterial line immediately above the sampling port; draw systemic (S) arterial sample from the arterial port line. Unclamp the line, resume dialysis. c. Measure the BUN in the arterial, venous, and systemic sample and calculate the percent recirculation. S - A X 100 % Recirculation = S-V 2. PNA (g/pro/day)=PCR (In patients with no significant protein losses) (PNA is the most accurate terminology) PNA (g/pro/day)=PCR + protein losses (In patients with significant urinary or dialytic protein losses) 3. PNA/PCR calculations are most accurate when calculated with UKM, but following the formulas can estimate PCR: PNA/PCR (without renal function) GU (mg/min) = (BUN2 x Vu2) - (BUN1 x Vu1) ÷ t PNA/PCR (gm/day) = 9.35 (GU) + 0.294(V) PNA/PCR (with renal function) GU (mg/min) = [(BUN2 x Vu2) - (BUN1 x Vu1)/t] + [ KrU x (BUN1 + BUN2/2) PNA/PCR = (6.49 x UNA) + (0.294 x V) (Borah equation) 4. nPNA = PNA ÷ V/0.58 5. Calculation of Residual Renal Urea Clearance (KrU) 2X wk KrU mL/min = Vu (mL) x Uu (mg/mL) 3x wk KrU ml/min = Vu (mL) x Uu (mg/mL) t x (0.25 BUN1 + 0.75 BUN2) mg/mL t x (0.16 BUN1 + 0.84 BUN2) V1 = estimated urea volume V2 = V1 + interdialytic wt gain t = interdialytic time in minutes Vu = urine volume (mL) during interdialytic period Uu = urine urea nitrogen mg/mL BUN2 mg/mL = Pre-BUN (2nd run of week) BUN1 mg/mL = Post-BUN (1st tx of week) References: Jindal KK, Goldstein MB: UKM in Chronic HD. Sem Dial 1:82, 1988 Gee C, Schroeffer C: Urea Kinetics in Nutritional Management of PreESRD, 1997

10-11

SUMMARY OF K/DOQI HEMODIALYSIS ADEQUACY RECOMMENDATIONS

1. Monthly formal urea kinetic modeling. 2. Minimum prescribed Kt/V of ≥1.3. 3. Minimum delivered Kt/V of ≥1.2 for thrice weekly dialysis. Twice weekly dialysis is not recommended. Although with a GFR >5 mL/min/1.73m2, reduced frequency may be tolerated, but residual urine output must be monitored diligently and frequency increased as needed to ensure adequate treatment. (see *Note below) 4. Rigorous blood sampling techniques as outlined in the K/DOQI Clinical Practice Guidelines. (Slow flow, stop pump) 5. Error analysis with timely modification of treatment parameters to correct underdialysis. 6. Research is needed for alternative methods of adequacy testing; more precise definition of adequate versus optimal dose of dialysis. * Note: It has been suggested that at minimum Kt/V of 2.3 be maintained in 2x week patients. Correspondence from Dr. Frank Gotch, San Francisco, CA, to Satellite Healthcare, March, 1997. Reference: NKF K/DOQI Clinical Practice Guidelines for HD Adequacy, Update 2000, Am J Kidney Dis. 37(1) Suppl 1, January, 2001

10-12

COMMON CAUSES OF DELIVERED Kt/V ≠ PRESCRIBED Problem Access Recirculation

Changes in Residual Renal Function

Dialyzer Capabilities

Excessive ID Weight Gain Double Pooling

Comment Average is 7% (Range 0-100%) can be affected by BFR, needle size, needle placement, graft placement (more proximal = less prone to recirculation). With transonic measurements recirculation should be “0.” Potential indicators: high or increasing venous pressure, black blood syndrome, Kt/V lower than predicted, large increase in kinetic volume, small needle size. Evaluate: Transonic access evaluation, two needle urea-based recirculation test, saline recirculation test, hydraulic compression test Failure to routinely measure urinary urea clearance results in underestimation of PNA, ignores a significant route of nitrogen elimination. Low preBUN is due to unmeasured urinary clearance, not low generation/intake. Potential Indicators: nPNA different than actual pro intake/other protein parameters. Evaluate: 24-48 hr urine collection, increased ID gain/preBUN as output decreases. Overestimation of clearance capabilities. Clearance can also be reduced by clotting (decr is not linearly related to loss of volume, 20% loss of volume in a hollow fiber dialyzer causes approximately a 10% loss of clearance). Potential indicators: Low Kt/V, high kinetic volume. Evaluate: Check reuse number, total cell volume (should be ≥80%), eliminate other causes of decreased clearance, recheck kinetics with a new dialyzer. Patients who cycle on the verge of pulmonary edema pretreatment to volume depletion posttreatment can have diluted pre-BUN, concentrated/normal post-BUN. Evaluate: ID weight gain/UF ave. See page 10-10. Potential indicators: High PNA, high Kt/V, high pre BUN, low kinetic V Evaluation: 30-minute post BUN, computer calculation of eKt/V. 10-13

STEPS TO ERROR ANALYSIS OF FORMAL HD UKM Initial analysis: 1. Compare the dialysis prescription to what was actually delivered. Was the actual BFR = prescribed BFR? Actual time=prescribed? Dialyzer = prescribed? Dialysate flow rate=prescribed? If the treatment parameters were not delivered as prescribed, the delivered Kt/V will be different than the prescribed Kt/V, but the kinetic volume and VSA will not be different unless other problems are also present. 2. Identify the abnormalities/compare: Prescribed Kt/V to delivered Kt/V. Volume from surface area or mean volume to kinetic (current) volume. nPNA/nPCR to actual protein intake and/or mean nPNA/nPCR. 3. Any significant error (high or low) or a delivered Kt/V < 1.2 should be investigated. In-depth analysis: 1. Review previous modeling to compare results and parameters. Were pre- and post-BUN levels similar to previous values? Drawn correctly? Be suspicious of very low post-BUN which may have been drawn from venous line. 2. Look for signs of recirculation (needle placement or size/notations of high or changing venous pressures). 3. Review ID weight gains and dry weight changes. Significant increase in hematocrit can make a small difference. 4. Note dialyzer reuse number, comments on visual inspection of dialyzer, and the tested total cell volume. 5. Clinical difficulties during the run (hypotensive episodes, access problems, off to bathroom, etc.). 6. There may be a combination of problems. When more than one problem is present, the indicators of one problem may be masked or canceled out by another problem. For example: If a patient has significant rebounding (which would normally cause a skew downward in kinetic volume) and a concurrent access problem (which would normally cause a skew upward in kinetic volume), the two might cancel each other out. This would result in the kinetic V being reasonably close to VSA or mean V and the delivered Kt/V similar to prescribed. Thus neither problem would be obvious. 10-14

HELPFUL INFORMATION FOR ANALYSIS OF UKM RESULTS: 1. Facility-specific blood sampling techniques. Timing affects values. Sampling should be appropriate for type of adequacy measure being used and consistent for all patients. (See K/DOQI Clinical Practice Guidelines for HD Adequacy) 2. Urine handling procedures. Refrigeration retards bacterial growth that can skew urea content in the urine. 3. Machine functions - do they track real treatment time, not just clock time? 4. Type and placement of access for each patient (from the medical record or daily log). 5. Routines for cannulation (distance between needles, orientation of needles). 6. Procedures and average reuse for each patient. 7. Average venous pressures for each patient. 8. Measured (not stated) patient height for accurate VSA calculation. 9. Actual dietary protein intake for comparison to the kinetically generated PNA. 10. Be sure that those who record the treatment parameters are recording actual delivered (time, BFR, DFR, etc.) treatment parameters, not just what the prescription says.

10-15

ERROR ANALYSIS FOR FORMAL UKM If Kt/V is < than expected (low clearance) and Kinetic V is > VSA or mean Volume A. Evaluate Clearance 1. Was blood flow really recorded as delivered? (Turned down or low because of poor access, increased gradually to prescribed level, but recorded at the prescribed level). 2. Is blood pump calibration correct? (Check other patients using the same equipment). 3. Is the blood pump stroke volume accurate? (Pre pump tubing collapsed with negative pre pump arterial pressure). 4. Clotting of dialyzer? Incorrect dialyzer data (would be consistently off, not just one time)? 5. Access recirculation? (Large increase in kinetic volume, high/changing venous pressures, needles too small). 6. Reuse problem? (Sudden drop in Kt/V, high reuse number, marginal TCV). 7. Was DFR set at the prescribed level and recorded correctly? (May not have been reset after the previous patient). 8. Blood lines or needles reversed? B. Evaluate Blood Sampling Procedure 1. Was the post BUN drawn too late (BUN begins to equilibrate quickly)? 2. Was the pre BUN sample diluted with saline? C. Evaluate Volume (V): With spvv UKM, a kinetic volume is determined each time. This kinetic or current volume reflects an estimate of body water based on the clearance of urea during the individual treatment. If the clearance of urea is less than expected with a certain dialysis prescription (BFR, DFR, time, frequency, dialyzer, patient VSA), it is assumed that the body of urea-laden body water is larger than the body water estimate from VSA. These changes indicate an error in the delivery of dialysis. Real changes in volume (not reflective of an error in the delivery of dialysis) occur if the patient is very muscular, obese, or has had a significant weight change such as an amputation. In a muscular patient, the kinetic volume may be higher than the anthropometric volume or VSA since muscle has a higher water content. If the patient has a high level of fat, the actual volume will usually be lower than the anthropometric volume or VSA because fatty tissue has a lower water content. Most formal kinetic modeling programs, provide only the VSA to compare to kinetic volume. If the UKM program saves data from session to session, a mean volume can be calculated. This provides a more accurate volume with which to compare the kinetic volume in those patients with atypical body composition where legitimate adjustments in body water are averaged into the mean over a few UKM sessions. 10-16

ERROR ANALYSIS FOR FORMAL UKM (Cont.) If Kt/V is lower or higher than prescribed, but volume is similar to VSA or mean volume

Evaluate Treatment Parameters - because the calculations are based on actual delivered treatment, if the time, BFR, DFR not delivered as prescribed, but are recorded accurately, formal UKM will use those actual delivered parameters to calculate the expected Kt/V and the V will not be skewed. The clearance of urea will be approximately equal to what is expected for the time, BFR, DFR, etc. If the treatment is not delivered as prescribed but is recorded as if it was, the volume will be skewed. 1. Was treatment time delivered as prescribed? Minor differences (i.e. 5 minutes) don’t impact results that much. 2. Was blood flow rate/dialysate flow rate equal to prescribed? (Same as above) 3. Was the correct dialyzer used? Monitor urine output: 1. Look for increased ID weight gain which signifies a decrease in output. 2. Look for changes in preBUN (will be higher as output decreases, if protein intake is stable). 3. May see increased albumin if patient has been nephrotic and then urine output drops.

10-17

ERROR ANALYSIS FOR FORMAL UKM (Cont.) If Kt/V is > than expected and volume is < than surface area or mean volume (clearance better than expected): A. Evaluate Clearance 1. Was the blood flow rate higher than prescribed? Dialysate flow rate higher than prescribed? 2. Was dialyzer performance better than expected? (Happens often if using in vivo rather than in vitro clearance figures). 3. Is there poor urea equilibration (double pooling)? (Common in small person with high blood flow/short time. Would normally also see a PNA higher than actual intake, high preBUN if the patient has slow equilibration). B. Evaluate Recorded Treatment Parameters 1. Were the delivered parameters recorded correctly? Is the machine properly calibrated? C. Evaluate Blood Sampling Procedure 1. Was the post BUN drawn from the venous line? (Often indicated by abnormally low post BUN, <10 mg/dL). 2. Was the post BUN drawn in accordance with the adequacy method used? Was the post BUN diluted with saline? 3. Was the timing of blood sampling correct? Immediate = falsely elevated Kt/V, inappropriate timing for any method of adequacy. 15 - 30 seconds after termination of treatment = most appropriate for formal single pool UKM Slow flow/stop pump technique (angioaccess recirculation resolved, urea rebound beginning) 2 - 3 minutes = low Kt/V/URR because of rebound, cardiopulmonary recirculation dissipated 5 - 10 minutes = low Kt/V or URR because of significant but incomplete urea rebound. 30 minutes = equilibrated for most patients, correlates with double pool model.

Other: Kt/V should be increased in proportion to mean nPNA if protein intake is appropriate or restriction of protein is not advisable (malnourished patient). Example: In a patient with a mean nPNA of > 1.1, the Kt/V should match the nPNA. Gotch FA, Keen ML: In Cognan MG: Introduction to Dialysis, Churchill & Livingston, NY, 1991

10-18

DIALYZER CHARACTERISTICS Type Conventional (refers to moderate urea clearances, small pores) High Efficiency (refers to urea clearance) High Flux (refers to UF coefficients and pore size) Membrane Cellulose

2-6 ml/ mmHg/hr

UFR

Surface Area 0.4-1.3 sq. meters

7-19 ml/ mmHg/ hr

1.3-2.2 sq. meters

20-60 ml/ mmHg/hr

1.2-1.9 sq. meters

Characteristics Names Least expensive; causes the most Cuprophane complement activation; contact with blood causes muscle protein catabolism indicated by aa in efferent blood; less Beta 2 removal * Somewhat more biocompatible because Cuprophane acetate/diacetate/ Modified Cellulose reactor sites are buffered with aa; less triacetate, cuprammonium rayon likely to cause aa release secondary to muscle protein catabolism* Most biocompatible, but to different Polyacrylonitrile (PAN) Synthetic degrees; polysulfone membranes are Polymethylmeth-acrylate endotoxin permeable so there is potential (PMMA) for inducing endotoxemia.* Polysulfone *Adverse effects are directly proportional to the amount of complement generated by the membrane, amount of complement generated is dependent on size and type of the membrane. Reference: Manufacturers’ Information 10-19

FORMULAS TO ESTIMATE EQUILIBRATED Kt/V Author Smye

Daugirdas-Schneditz Rate Adjustment Equation

Formula Ceq= Co x EXP (-[T/T-Ts]) x Ln [Cs/Ct] Ceq = equilibrated post-/ dialysis BUN Co = pre-dialysis BUN Cs = mid-dialysis (70 minute) BUN Ct = BUN at the end of dialysis T = duration of treatment Ts = time at which the mid-dialysis BUN is drawn EXP = exponential of bracketed terms Ln = natural logarithm of bracketed terms *arterial post BUN from A-V access: art. eKt/V = art. spKt/V - (0.6 x art. spKt/V/t) + 0.03 venovenous access post BUN: ven. eKt/V=ven. spKt/V - (0.4 x ven. spKt/V/t) + 0.02 eKt/V = equilibrated Kt/V spKt/V = single pool Kt/V t - treatment time in hours * Mathematical relationship between eKt/V and spKt/V depends on location of access and blood sampling site.

References: Daugirdas JT, et al: Comparison of models to predict the equilibrated Kt/V in the HEMO study. J Am Soc Nephrol 6:596, 1995 10-20

FORMULAS FOR OTHER MEASURES OF HD ADEQUACY Measure Natural Logarithm Formula URR

Formula Kt/V = -Ln (R - 0.008 X time) + (4 - 3.5 x R) x ultrafiltration volume in L¸ post dialysis weight in kg (Where R = post BUN divided by pre BUN) URR = 100 X (1- post-BUN/pre-BUN) With significant interdialytic weight gains and subsequent ultrafiltration, the URR has variable correlations to Kt/V.

Targets Same as for formal UKM ≥ 65% (approx. = Kt/V of 1.2)

Reference: NKF K/DOQI Clinical Practice Guidelines for HD Adequacy, Update 2000, Am J Kidney Dis. 37(1) Suppl 1, January, 2001

10-21

DAILY HEMODIALYSIS Daily short dialysis has been used by various invesitgators since 1967. It has been consistently associated with marked improvement in patient well being. Daily short dialysis and slow nocturnal dialysis are both seen as superior standards of care. The following clinical benefits have been reported: Increased hematocrit with decreased need for erythropoietin Enhanced blood pressure control and decreased need for pharmacologic blood pressure therapy Increased protein intake and body weight (intake went from 1.0 gm/kg to 1.3 gm/kg) Significantly fewer complications of dialysis (hypotension, headaches, cramps, post-dialysis fatigue) Increased energy and patient-reported improvement in quality of life Assumed decrease in mortality Little or no need for diet restriction (research will help define nutrient losses and replacement needs) Little or no need for phosphate binders (no patients needed binders, 70% required phosphorus supplementation) Focus is on long-term healthy eating and activity/exercise as recommended for those without CKD. This becomes even more important as we are hopeful that these patients will live longer on dialysis therapy. Adequacy testing for daily short HD and slow nocturnal HD is in development stages. It is possible to modify formal UKM calcuations to consider the increased frequency of dialysis. Since formal urea kinetic modeling was deemed by K/DOQI to be the best method of adequacy testing for thrice weekly HD, it is logical that we should apply the same standard to more frequent dialysis. Some use a simple adaptation of URR, however, the same limitations of URR in thrice weekly dialysis, would likely apply to its use in more frequent HD therapy (see page 10-6). Reference: McPhatter LL, Lockridge RS: Nutritional Advantages of Nightly Home HD. NNI16 (3):31-36, 2002 Gotch FA, Levin NW: Daily Dialysis: The Long and Short of It. (Submitted for publication) 10-22

PD ADEQUACY FORMULAS

Patient Example:

1. 2.

Calculate TBW and BSA (see page 10-9) Calculate residual urea clearance: (Uu x Uv)/(1440 x Su)

3.

Calculate residual (urinary) Kt/V: (Urea clearance x 1440 x 7)/(V x 1000)

4.

Calculate dialysis Kt/V: (Du/Su x Dv x 7)/(V x 1000)

5.

Calculate total Kt/V: Residual Kt/V + Dialysis Kt/V

6.

Calculate creatinine clearance: (Ucr x Uv )/(1440 x Scr)

7.

Calculate mean GFR: (Residual CrCl + Residual urea clearance)/2

8.

Calculate Urinary CrCl: (Mean GFR x 1440 x 7)/1000

9.

Calculate Dialysis CrCl: (Dcr /Scr x Dv x 7)/1000

Urea mg/dL Creat mg/dL Volume mL Urine: 333(Uu) 136 (Ucr) 475 (Uv) 6.91 (Scr) Serum: 60 (Su) 4.5 (Dcr) 12485 (Dv) Dialysate: 52 (Du) (Total effluent) 1. BSA = 1.88 m2 Total Body Water or Volume (V) = 40.4 2. Resid. urea clear = (333 x 475)/(60 x 1440) = 158175/86400 or 1.83 mL/min 3. Residual Kt/V = (1.83 x 1440 x 7)/(40.4 x 1000) = 18446.4/40400 or 0.46/wk 4. Dialysis Kt/V = (52/60 x 12485 x 7)/40.4 x 1000 = 75771.47/40400 or 1.88/wk 5. Total Kt/V = 0.46 + 1.88 or 2.33 6. Residual CrCl = (136 x 475)/(1440 x 6.91) = 64600/9950 or 6.49 g/d 7. Mean GFR = 2.33 + 1.83 or 4.16 mL/min 8. Urinary CrCl = (4.16 x 1440 x 7)/1000 = 41932.8/1000 or 41.9 L/wk 9. Dialysis CrCl = (4.5/6.91 x 12485 x 7)/1000 = 0.651 x 12485 x 7/1000 = 56894.2/1000 or 56.9 l/wk 10.Total CrCl = 41.9 + 56.9 or 98.8 l/wk

10. Calculate total CrCl: Urinary CrCl + Dialysis CrCl 11. Normalize to patient BSA Total CrCl x 1.73/Pt BSA

11.Normalized CrCl

= 98.8 x 1.73/1.88 or 90.9 l/wk

10-23

PD ADEQUACY FROMUALS (Cont.)

Patient Example: (Same values as 10-23)

1.

1. UNA = (52/100 x 12485)+(333/100 x 475)/1000 UNA = 6492.2 +1581.75/1000 UNA = 8.07

Calculate UNA (Du/100 x Dv) + (Uu/100 x Uv)/1000

2. Determine if the patient has protein losses >15 g/d. Potential: Nephrotic patients, those with high transport membranes, and those whose clinical picture doesn’t correspond with chemistries (well nourished, eating well, but low protein parameters.) Obtain 24 hr protein levels for dialysate and urine. Convert to gm/day. Dpro x (Dv/100) + Upro x (Uv/100)/1000

2. Obtain 24 hour protein levels from urine and dialysate. Sample patient has 117 mg/dL protein in dialysate (Dpro) and 107 mg/dL in urine (Upro). Pro loss gm/d =117x(12485/100)+107x(475/100)/1000 Pro loss gm/d = (117 x 124.9) + (107 x 4.75)/1000 Pro loss gm/d = (14613.3 + 508.25)/1000 Total pro loss g/d = 15.1 g

3.

Calculate PNA if protein loss >15 g/d PCR = (6.49 x UNA) + (0.294 x V) PNA = PCR + Protein losses

3. PNA PNA PNA PNA

= (6.49 x 8.07) + (0.294 x 40.4) + 24 hr pro loss = 52.4 + 11.8 + 15.1 = 64.2 + 15.1 = 79.3 gm/d

4.

Calculate PD PNA (if protein loss <15 gm) PNA g/d (Incorporates ave. PD protein loss of 7.3 g/d) 10.76 x (0.69 x UNA + 1.46)

4. PNA = 10.76 x (0.69 x 8.07 + 1.46)(if pro loss < 25 gm) PNA = 10.76 x 7.031 PNA = 75.65 gm/d

5.

Calculate Normalized PNA (nPNA) nPNA = PNA/(V/0.58)

5. nPNA = nPNA = nPNA =

75.65/(40.4/0.58) 75.65/69.57 1.09 gm/kg/d

10-24

SUMMARY OF K/DOQI PD ADEQUACY GUIDELINES 1. 2. 3.

4. 5.

6. 7. 8.

Initiate dialysis incrementally to maintain a total Kt/V of at least 2.0 and nPNA of at least 0.8 gm/kg. PD adequacy testing should be performed within one month and at least 1 additional time between month 2 and 6 (depends on consistency from initial results), and then q 4 months. PD targets are based on the type of PD therapy with continuous, longer dwell time (CAPD) targets lower than those for interrupted (NIPD) or shorter dwell therapies (APD). The Kt/V and CrCl L/wk/1.732 targets are: CAPD 2.0/60 L for high and high average transporter and 2.0/50L for low and low average transporters, NIPD 2.2/66 L, CCPD or APD 2.1/63 L. If total daily creatinine excretion differs from baseline by ≥15%, error analysis should be initiated (patient compliance, dialysate/urine collection procedures/accuracy, altered peritoneal transport characteristics). Nutritional status of adult PD patients should be assessed at least every 4 months using SGA (1-34 to 1-41) and PNA (See page 10- 24). Evaluate pediatric patients using PNA and other nutritional assessment techniques that have been demonstrated as accurate in pediatric patients. Identify and correct patient or staff errors in meeting minimum targets. Regularly measure clinical outcomes (patient survival, technique survival, hospitalization rates, patient-based QOL, albumin, Hgb/Hct, nPNA, and school attendance/developmental progress in pediatric patients). Indications for PD (pt preference, medical complications/no assistant for home HD). Contraindications for PD: loss of peritoneal function, inability to perform and no assistant, mechanical defects/leaks, body size, severe malnutrition, diverticular/bowel disease Reasons to change to HD: consistent adequacy failure, unmanageable hypertriglyceridemia, recurrent peritonitis/complications, technical/mechanical problems, severe malnutrition.

Reference: NKF K/DOQI Clinical Practice Guidelines for PD Adequacy, Update 2000, Am J Kidney Dis 37(1) Suppl 1, January 2001 10-25

KINETIC MODELING FORMULAS FOR CKD NOT ON DIALYSIS 1. Urea Clearance (KrU) - urine urea x urine volume

BUN

time

Creatinine Clearance (CrCl) = urine creatinine x urine volume serum creatinine time 2. Approximate GFR mL/min = KrU mL/min + CrCl mL/min 2 3. Urea Generation Rate (GU) = KrU x BUN concentration Creatinine Generation (GCr) = KrCr x Creatinine concentration 4. PNA (PCR) = 9.35 (GU) + 11 5. nPNA (normalized protein equivalent of total nitrogen appearance) = PNA/Lean Body Weight (LBW) LBW = Total Body Water/0.58 (TBW see 10-9) 6. PNA is the more accurate terminology and: PNA = PCR (if there are no urinary protein losses) PNA = PCR + urinary protein losses Reference: CRN of Northern California/Northern Nevada, Pre-End Stage Renal Disease: A Guide for the Professional Nutritionist, 1986. 10-26

NUTRITION INTERVENTION BASED ON nPNA HD nPNA

Significance

Nutritional Intervention

>1.4

Excessive intake, excessive LBV protein, or catabolism

1.2

Ideal

0.7 - 0.9

Inadequate protein intake, inadequate treatment also increases risk of morbidity/ mortality.

Assess dietary intake, decrease protein intake if excessive and patient is well nourished. Look for other problems such as catabolism (change in weight/ protein status). Encourage patient to continue current intake if protein status/weight are acceptable Assess dietary intake, counsel patient to increase protein/calorie intake if appropriate. Look for signs of anabolism (change in wt/protein status). Consider oral nutritional supplement. Assess dialysis adequacy. Begin oral supplement as tolerated, encourage intake, assess adequacy. Aggressive nutrition support as appropriate. Routinely assess adequacy at all stages.

0.6 - 0.69 <0.59

PD nPNA >1.5

1.2 - 1.3 <1.2

<0 .8

<0.60

10-27

GLOMERULAR FILTRATION RATE (GFR) CALCULATIONS MDRD Equation1: GFR = 170 x serum creatinine -0.999 x SUN -0.17 x Age-0.176 x serum albumin0.318 x 0.762 if female0.762 x 1.18 if black race Modified MDRD Equation2: 186 x sCR-1.154 x age -0.203 x 0.742 if female x 1.212 if black race Cockroft-Gault Equation3: GFR = [(140-age) x body weight (kg) x 0.85 if female] / [72 x serum creatinine (mg/dL)] Reference:

1

Levy AS, Bosch JP, Lewis JB, et al: A more accurate method to estimat GFR from serum creatinine: A new prediction equation. MDRD Study Group, Ann Intern Med 130:461-470, 1999 Levey AS, Greene T, Kusek JW, et al. A simplified equation to predict glomerular filtration rate from serum creatinine. J Am Soc Nephro 11, 2000 3 Walser M: Assessing renal function from creatinine measurements in adults with chronic kidney failure. Am J Kidney Dis. 32:23-31, 1998 2

ESTIMATION OF CREATININE CLEARANCE Male CrCl =

Wt in kg x (140 - age) 72 x serum creatinine (mg/dL) Female CrCl = Use above formula and multiply by 0.85 Paraplegics = Use above formula and multiply by 0.80 Quadriplegics = Use above formula and multiply by 0.60 References: Schrier R, Ed: Manual of Nephrology, Little Brown and Co., Boston, 1990 Daugirdas JT, Ing TS: Handbook of Dialysis, Little, Brown & Co., 2000

10-28

Chapter 11: SPECIAL CONSIDERATIONS FOR THE PEDIATRIC PATIENT

Notes:

11-2

NUTRITION ASSESSMENT OF THE PEDIATRIC PATIENT There are a number of clinical issues that may differ in pediatric patients. This chapter is not all inclusive, but highlights the major differences in assessment parameters for pediatric patients. Notations in this chapter indicate where additional information is included within the adult assessment chapters. If a specific topic is not addressed, it is because the pediatric editors determined that there were no significant differences or that the topic was not applicable to pediatric patients. For more detail on pediatric nutritional assessment, please consult the reference list at the end of this chapter.

11-3

PRACTICAL STEPS TO NUTRITION ASSESSMENT OF PEDIATRIC PATIENTS 1.

2.

3.

4. 5.

Follow-up must be more frequent, depending on age and body needs. Dialysis patient - Monthly Transplant - Every 1-4 weeks Pre-dialysis - Monthly, if failure to thrive is an issue Person(s) to Interview: Infant/toddler - primary care giver (parent, grandparent, guardian) School age children - both child and primary care giver Adolescent - adolescent with corroboration of primary care giver, as needed Physical assessment to document growth must include routine evaluation of: Length (laying) or height (standing) Weight Head Circumference (age 36 months and younger) Use standardized measuring techniques (Queen P: Handbook of Pediatric Nutrition, Aspen Publications, pg. 12, 1993) Plot results on age and sex appropriate standard or premature growth charts as applicable to determine percentiles of: Weight for age Height for age Head Circumference Weight for height Height age (Age 36 months and below) Arm anthropometry (Frisancho tables) Mid-arm circumference Triceps Skinfold Infants (less than 24 months) include: Gestational age Birth weight/length Evaluate current feeding skills/abilities: Sucking (infant) Chewing/swallowing Self-feeding (finger foods/spoon/bottle/cup) Determine status of toilet training/assess: Urine output Stool output (frequency, color, consistency)

Note: SGA has not been validated in pediatric patients. 11-4

ASSESSMENT OF PROTEIN/ENERGY STATUS IN PEDIATRIC PATIENTS (K/DOQI) Initial intense nutritional counseling for appropriate caretakers on individualized plan of care including standard measurements of growth and physical development. This should be developed early in treatment, reevaluated frequently, and modified according to progress (minimally every 3-4 months). Appropriate Methods for Evaluation of Protein/Energy Status Dietary interview Serum Albumin Height/length Estimated dry wt Weight/Height Index MAC, MAMC, MAMA Skinfold thickness Head Circumference (< 3 yrs) Standard Deviation Score for height for chronological age Urea Kinetic Modeling

Frequency* <2 yrs

Frequency* >2 years

Monthly Monthly Monthly Monthly Monthly q 3-4 mo NA Monthly

q 3-4 mo Monthly q 3-4 mo q 3-4 mo q 3-4 mo q 3-4 mo q 3-4 mo q 3-4 mo to 36 mo

Monthly q 3-4 mo PD

q 3-4 mo q 3-4 mo PD

Other

Acid Base Balance: Maintain serum CO2: ≥ 22 mmol/L With administration of alkali therapy or change in dialysate concentration

PNA not validated

* Frequency of assessment should increase with changes in status such as persistent anorexia or GI symptoms, change in social structure, decrease in dry weight or height for weight. Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6), Suppl 2, June, 2000 11-5

MID-ARM CIRCUMFERENCE (MAC) REFERENCE VALUES (cm) Age Years 1-1.9 2-2.9 3-3.9 4-4.9 5-5.9 6-6.9 7-7.9 8-8.9 9-9.9 10-10.9 11-11.9 12-12.9 13-13.9 14-14.9 15-15.9 16-16.9 17-17.9 18-18.9 19-24.9 Reference:

5 142 141 150 149 153 155 162 162 175 181 186 193 194 220 222 244 246 245 262

Pediatric Male % Standard 10 25 50 75 90 146 150 159 170 176 145 153 162 170 178 153 160 167 175 184 154 162 171 180 186 160 167 175 185 195 159 167 179 188 209 167 177 187 201 223 170 177 190 202 220 178 187 200 217 249 184 196 210 231 262 190 202 223 244 261 200 214 232 25.4 282 211 228 247 26.3 286 226 237 253 28.3 303 229 244 264 28.4 311 248 262 278 30.3 324 253 267 285 30.8 336 260 276 297 32.1 353 272 288 308 33.1 355

95 183 185 190 192 204 228 230 245 257 274 280 303 301 322 320 343 347 379 372

5 138 142 143 149 153 156 164 168 178 174 185 194 202 214 208 218 220 222 221

Pediatric Female % Standard 10 25 50 75 90 142 148 156 164 172 145 152 160 167 176 150 158 167 175 183 154 160 169 177 184 157 165 175 185 203 162 170 176 187 204 167 174 183 199 216 172 183 195 214 247 182 194 211 224 251 182 193 210 228 251 194 208 224 248 276 203 216 237 256 282 211 223 243 271 301 223 237 252 272 304 221 239 254 279 300 224 241 258 283 313 227 241 264 295 324 227 241 258 281 312 230 247 265 290 319

95 177 184 189 191 211 211 231 261 260 265 303 294 338 322 322 334 350 325 345

Frisancho R: Anthropometric Standards for the Assessment of Growth andNutritional Status, The University of Michigan Press, Ann Arbor, MI, 1993 11-6

TRICEPS SKINFOLD THICKNESS (mm) Age Years 1-1.9 2-2.9 3-3.9 4-4.9 5-5.9 6-6.9 7-7.9 8-8.9 9-9.9 10-10.9 11-11.9 12-12.9 13-13.9 14-14.9 15-15.9 16-16.9 17-17.9 18-18.9 19-24.9

5 6 6 6 6 6 5 5 5 6 6 6 6 5 4 4 4 5 4 4

Pediatric Male % Standard 10 25 50 75 90 7 8 10 12 14 7 8 10 12 14 7 8 10 11 14 6 8 9 11 12 6 8 9 11 14 6 7 8 10 13 6 7 9 12 15 6 7 8 10 13 6 7 10 13 17 6 8 10 14 18 6 8 11 16 20 6 8 11 14 22 5 7 10 14 22 5 7 9 14 21 5 6 8 11 18 5 6 8 12 16 5 6 8 12 16 5 6 9 13 20 5 7 10 15 20

95 16 15 15 14 15 16 17 16 18 21 24 28 26 24 24 22 19 24 22

5 6 6 7 7 6 6 6 6 8 7 7 8 8 9 8 10 10 10 10

Pediatric Female % Standard 10 25 50 75 90 95 7 8 10 12 14 16 8 9 10 12 15 16 8 9 11 12 14 15 8 8 10 12 14 16 7 8 10 12 15 18 6 8 10 12 14 16 7 9 11 13 16 18 8 9 12 15 18 24 8 10 13 16 20 22 8 10 12 17 23 27 8 10 13 18 24 28 9 11 14 18 23 27 8 12 15 21 26 30 10 13 16 21 26 28 10 12 17 21 25 32 12 15 18 22 26 31 12 13 19 24 30 37 12 15 18 22 26 30 11 14 18 24 30 34

Reference: Frisancho R. Anthropometric Standards for the Assessment of Growth and Nutritional Status, The University of Michigan Press, Ann Arbor, MI, 1993 11-7

2-7:

ESTIMATED MID-ARM MUSCLE CIRCUMFERENCE Age Years 1-1.9 2-2.9 3-3.9 4-4.9 5-5.9 6-6.9 7-7.9 8-8.9 9-9.9 10-10.9 11-11.9 12-12.9 13-13.9 14-14.9 15-15.9 16-16.9 17-17.9 18-18.9 19-24.9

5 110 111 117 123 128 131 137 140 151 156 159 167 172 189 199 213 224 226 238

Pediatric Male % Standard 10 25 50 75 90 113 119 127 135 144 114 122 130 140 146 123 131 137 143 148 126 133 141 148 156 133 140 147 154 162 135 142 151 161 170 139 151 160 168 177 145 154 162 170 182 154 161 170 183 196 160 166 180 191 209 165 173 183 195 205 171 182 195 210 223 179 196 211 226 238 199 212 223 240 260 204 218 237 254 266 225 234 249 269 287 231 245 258 273 294 237 252 264 283 298 245 257 273 289 309

95 147 150 153 159 169 177 180 187 202 221 230 241 245 264 272 296 312 324 321

5 105 111 113 115 125 130 129 138 147 148 150 162 169 174 175 170 175 174 179

Pediatric Female % Standard 10 25 50 75 90 111 117 124 132 139 114 119 126 133 142 119 124 132 140 146 121 128 136 144 152 128 134 142 151 159 133 138 145 154 166 135 142 151 160 171 140 151 160 171 183 150 158 167 180 194 150 159 170 180 190 158 171 181 196 217 166 180 191 201 214 175 183 198 211 226 179 190 201 216 232 178 189 202 215 228 180 190 202 216 234 183 194 205 221 239 179 191 202 215 237 185 195 207 221 236

95 143 147 152 157 165 171 176 194 198 197 223 220 240 247 244 249 257 245 249

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6), Suppl 2, June, 2000 11-8

FORMULA FOR MID-ARM MUSCLE CIRCUMFERENCE AND MID-ARM MUSCLE AREA MAMC = MAC – (3.14 x TSF in cm) [MACcm – (3.14 x TSFmm)2 /4 X 3.14] – 10 MAMA for females: [MACcm – (3.14 x TSFmm)2 /4 X 3.14] – 6.5 MAMA for males:

FORMULAS FOR CALCULATING STANDARD DEVIATION SCORES SDS = [Pt actual height or weight] – 50th percentile value/standard deviation of control subjects. SDS for height or weight compares growth rates over specific time intervals. Note: Approximately 95% of healthy North American children fall within a SDS score of 2 SD An SDS score of > positive 2.0 or > a negative 2.0 is associated with abnormal ht/wt

LENGTH FOR INFANTS (For calculating SDS Scores) Boys Length cm 50.5 61.1 67.8 72.3 76.1 79.4 82.4 85.1

Age 0 0.25 0.5 0.75 1 1.25 1.5 1.75

SD 2.29 2.65 2.69 2.65 2.70 2.85 3.04 3.23

Girls Length cm Std Dev 49.9 2.17 59.5 2.49 65.9 2.64 70.4 2.73 74.3 2.84 77.8 2.95 80.9 3.07 83.8 3.18

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure.Am J Kidney Dis 35(6), Suppl 2, June, 2000 11-9

50 PERCENTILE FOR HEIGHT IN BOYS (For Calculating SDS Scores for Height) TH

Age 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

0 86.8 94.9 102.9 109.9 116.1 121.7 127.0 132.2 137.5 143.3 149.7 156.5 163.1 169.0 173.5 176.2 176.8

Reference:

0.1 87.5 95.7 103.6 110.5 116.7 122.2 127.5 132.7 138.1 143.9 150.4 157.2 163.7 169.5 173.8 176.3 176.8

0.2 88.2 96.6 104.4 111.2 117.3 122.8 128.0 133.2 138.6 144.5 151.0 157.9 164.3 170.0 174.2 176.4 176.8

0.3 88.9 97.4 105.1 111.8 117.8 123.3 128.6 133.8 139.2 145.2 151.7 158.5 164.9 170.5 174.5 176.5 176.8

0.4 89.7 98.3 105.9 112.5 118.4 123.8 129.1 134.3 139.7 145.8 152.3 159.2 165.6 171.0 174.9 176.6 176.8

0.5 90.4 99.1 106.6 113.1 119.0 124.4 129.6 134.8 140.3 146.4 153.0 159.9 166.2 171.5 175.2 176.7 176.8

0.6 91.3 99.8 107.3 113.7 119.5 124.9 130.1 135.3 140.9 147.0 153.7 160.5 166.8 171.9 175.4 176.7 176.8

0.7 92.2 100.6 107.9 114.3 120.1 125.4 130.6 135.9 141.5 147.7 154.4 161.2 167.3 172.3 175.6 176.7 176.8

0.8 93.1 101.4 108.6 114.9 120.6 125.9 131.2 136.4 142.1 148.4 155.1 161.8 167.9 172.7 175.8 176.8 176.8

0.9 94.0 102.1 109.2 115.5 121.2 126.5 131.7 136.9 142.7 149.0 155.3 162.6 168.4 173.1 176.0 176.8 176.8

NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-10

STANDARD DEVIATION VALUES FOR HEIGHT IN BOYS (For calculating SDS scores) Age 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

0 3.6 3.95 4.28 4.56 4.8 5.08 5.35 5.74 6.20 6.78 7.51 8.18 8.48 8.11 7.39 6.81 6.66

Reference:

0.1 3.63 3.99 4.31 4.58 4.82 5.10 5.39 5.78 6.26 6.86 7.58 8.23 8.46 8.04 7.32 6.79 6.66

0.2 3.67 4.02 4.34 4.61 4.85 5.13 5.43 5.83 6.32 6.93 7.65 8.28 8.43 7.98 7.25 6.76 6.66

0.3 3.7 4.06 4.38 4.63 4.87 5.15 5.48 5.87 6.38 7.01 7.73 8.32 8.41 7.91 7.19 6.74 6.66

0.4 3.74 4.09 4.41 4.66 4.89 5.18 5.52 5.92 6.44 7.08 7.79 8.37 8.38 7.85 7.12 6.71 6.66

0.5 3.77 4.13 4.44 4.68 4.92 5.20 5.56 5.96 6.50 7.16 7.87 8.42 8.36 7.78 7.05 6.69 6.66

0.6 3.81 4.28 4.46 4.70 4.95 5.23 5.59 6.0 6.56 7.23 7.93 8.43 8.31 7.70 7.0 6.68 6.66

0.7 3.84 4.43 4.49 4.73 4.98 5.26 5.63 6.06 6.61 7.3 7.99 8.44 8.26 7.62 6.95 6.68 6.66

0.8 3.88 4.58 4.51 4.75 5.02 5.29 5.67 6.10 6.67 7.37 8.06 8.46 8.21 7.55 6.91 6.67 6.66

0.9 3.91 4.73 4.54 4.78 5.05 5.32 5.70 6.15 6.72 7.44 8.12 8.47 8.16 7.47 6.86 6.67 6.66

NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-11

50 PERCENTILE FOR HEIGHT IN GIRLS (Used to calculate SDS Scores for Height) th

Age 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

0 86.8 94.1 101.6 108.4 114.6 120.6 126.4 132.2 138.3 144.8 151.5 157.1 160.4 161.8 162.4 163.1 163.7

Reference:

0.1 87.4 94.9 102.3 109.0 115.2 121.1 126.9 132.8 138.9 145.5 152.1 157.5 160.6 161.9 162.5 163.2 163.7

0.2 88.1 95.6 102.9 109.7 115.8 121.8 127.6 133.1 139.6 146.2 152.7 157.9 160.7 161.9 162.5 163.2 163.7

0.3 88.7 97.1 104.3 110.9 117.0 122.9 128.7 134.6 140.9 147.5 151.7 158.5 164.9 170.5 174.5 176.5 176.8

0.4 89.7 98.3 105.9 112.5 118.4 123.8 129.1 134.3 139.7 145.8 153.9 158.6 161.0 162.0 162.6 163.3 163.7

0.5 90.0 97.9 105.0 111.6 117.6 123.5 129.3 135.2 141.5 148.2 154.6 159.0 161.2 162.1 162.7 163.4 163.7

0.6 90.8 99.6 105.7 112.2 118.2 124.1 129.9 135.8 142.2 148.9 155.1 169.3 161.3 162.2 162.8 163.5 163.7

0.7 91.6 99.4 106.4 112.8 118.8 124.7 130.5 136.4 142.8 149.5 155.6 159.6 161.4 162.2 162.9 163.5 163.7

0.8 92.5 100.1 107.0 113.4 119.4 125.2 131.0 137.1 143.2 150.2 156.1 159.8 161.6 162.3 162.9 163.6 163.7

0.9 93.3 100.9 107.7 114.0 120.0 125.8 131.6 137.7 144.1 150.8 156.6 160.1 161.7 162.3 163.0 163.6 163.7

NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-12

STANDARD DEVIATION VALUES FOR HEIGHT IN GIRLS (For calculation of SDS scores) Age 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

0 3.65 3.74 4.04 4.41 4.89 5.38 5.87 6.32 6.69 6.90 6.96 6.96 6.87 6.78 6.60 6.32 6.08

0.1 3.65 3.77 4.08 4.56 4.94 5.43 5.92 6.36 6.71 6.91 6.96 6.95 6.86 6.76 6.57 6.29 6.08

0.2 3.65 3.80 4.11 4.51 4.99 5.48 5.97 6.39 6.74 6.92 6.96 6.95 6.86 6.74 6.54 6.26 6.08

0.3 3.65 3.83 4.15 4.55 5.04 5.52 6.01 6.43 6.76 6.94 6.96 6.94 6.85 6.73 6.50 6.23 6.08

0.4 3.65 3.86 4.18 4.60 5.09 5.57 6.06 6.46 6.79 6.95 6.96 6.94 6.85 6.71 6.47 6.20 6.08

0.5 3.65 3.89 4.22 4.65 5.14 5.62 6.11 6.50 6.81 6.96 6.96 6.93 6.84 6.69 6.44 6.17 6.08

0.6 3.67 3.92 4.26 4.69 5.19 5.67 6.15 6.54 6.83 6.96 6.96 6.92 6.83 6.67 6.42 6.15 6.08

0.7 3.69 3.95 4.29 4.75 5.24 5.72 6.19 6.58 6.85 6.96 6.96 6.91 6.82 6.65 6.39 6.13 6.08

0.8 3.7 3.98 4.33 4.79 5.28 5.77 6.24 6.61 6.86 6.96 6.96 6.89 6.80 6.64 6.37 6.12 6.08

0.9 3.72 4.01 4.37 4.84 5.33 5.82 6.28 6.65 6.88 6.96 6.96 6.88 6.79 6.62 6.34 6.10 6.08

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-13

50TH PERCENTILES FOR WEIGHT IN BOYS (For calculation of SDS scores) Age 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

0 12.34 14.60 16.69 18.67 20.69 22.85 25.30 28.13 31.44 35.30 39.78 44.95 50.77 56.71 62.10 66.31 68.88

0.1 12.58 14.81 16.89 18.87 20.90 23.09 25.56 28.45 31.81 35.73 40.28 45.52 51.37 57.35 62.56 66.60 68.88

0.2 12.81 15.03 17.09 19.07 21.11 23.32 25.82 28.77 32.18 36.16 40.78 46.09 51.97 57.99 63.02 66.90 68.88

0.3 13.05 15.25 17.29 19.27 21.32 23.56 26.08 29.09 32.56 36.59 41.27 46.67 52.56 58.63 63.47 67.19 68.88

0.4 13.30 15.46 17.49 19.47 21.53 23.79 26.34 29.41 32.93 37.03 41.77 47.24 53.16 59.27 63.93 67.49 68.88

0.5 13.52 15.68 17.69 19.67 21.74 24.03 26.66 29.73 33.30 37.46 42.27 47.81 53.76 59.51 64.39 67.78 68.88

0.6 13.74 15.88 17.89 19.87 21.96 24.28 26.95 30.07 33.70 37.92 42.81 48.40 54.35 60.03 64.77 68.00 68.88

0.7 13.95 16.08 18.08 20.08 22.18 24.54 27.25 30.41 34.10 38.39 43.34 48.99 54.94 60.55 65.16 68.22 68.88

0.8 14.17 16.29 18.28 20.28 22.41 24.79 27.54 30.76 34.50 38.85 43.88 49.59 55.53 61.06 65.54 68.44 68.88

0.9 14.38 16.49 18.47 20.49 22.63 25.05 27.84 31.09 34.90 39.32 44.41 50.18 56.12 61.58 65.93 68.66 68.88

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-14

STANDARD DEVIATION VALUES FOR WEIGHT IN BOYS (For calculation of SDS scores) Age 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

0 1.52 1.74 2.02 2.38 2.86 3.49 4.29 5.27 6.36 7.50 8.58 9.54 10.31 10.94 11.51 11.91 12.70

0.1 1.54 1.77 2.05 2.42 2.92 3.59 4.38 5.38 6.47 7.61 8.68 9.62 10.38 10.99 11.57 12.01 12.70

0.2 1.56 1.79 2.08 2.47 2.98 3.70 4.48 5.49 6.59 7.72 8.78 9.69 10.44 11.06 11.63 12.11 12.70

0.3 1.58 1.82 2.12 2.51 3.04 3.81 4.57 5.59 6.70 7.83 8.88 9.77 10.51 11.11 11.68 12.21 12.70

0.4 1.60 1.84 2.15 2.56 3.10 3.91 4.67 5.70 6.82 7.94 8.98 9.85 10.57 11.17 11.74 12.31 12.70

0.5 1.62 1.87 2.18 2.60 3.16 4.02 4.76 5.81 6.93 8.05 9.08 9.93 10.64 11.23 11.80 12.41 12.70

0.6 1.64 1.90 2.22 2.65 3.23 4.07 4.86 5.92 7.04 8.16 9.17 10.01 10.70 11.29 11.82 12.47 12.70

0.7 1.67 1.93 2.26 2.70 3.29 4.13 4.96 6.03 7.16 8.26 9.26 10.08 10.76 11.34 11.84 12.53 12.70

0.8 1.69 1.96 2.30 2.76 3.36 4.18 5.07 6.14 7.27 8.37 9.36 10.16 10.82 11.39 11.87 12.58 12.70

0.9 1.72 1.99 2.34 2.81 3.42 4.24 5.17 6.25 7.39 8.47 9.45 10.23 10.88 11.45 11.89 12.64 12.70

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-15

50 PERCENTILES FOR WEIGHT IN GIRLS (For calculation of SDS scores) TH

Age 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

0 11.80 14.10 15.96 17.66 19.52 21.84 24.84 28.46 32.55 36.95 41.53 46.10 50.23 53.68 55.89 56.69 56.62

0.1 12.05 14.29 16.13 17.84 19.74 22.12 25.19 28.86 32.98 37.41 41.99 46.53 50.64 53.94 56.00 56.69 56.62

0.2 12.29 14.49 16.30 18.02 19.96 22.41 25.54 29.26 33.42 37.86 42.45 46.96 51.01 54.19 56.11 56.70 56.62

0.3 12.54 14.68 16.47 18.20 20.17 22.69 25.88 29.65 33.85 38.32 42.92 47.39 51.37 54.45 56.22 56.70 56.62

0.4 12.78 14.88 16.64 18.38 20.39 22.98 26.23 30.05 34.29 38.77 43.38 47.83 51.74 54.70 56.33 56.71 56.62

0.5 13.03 15.07 16.81 18.56 20.61 23.26 26.58 30.45 34.72 39.23 43.84 48.26 52.10 54.96 56.44 56.71 56.62

0.6 13.24 15.25 16.98 18.75 20.86 23.58 26.96 30.87 35.17 39.69 44.29 48.66 52.42 55.15 56.49 56.69 56.62

0.7 13.46 15.43 17.15 18.94 21.10 23.89 27.33 31.29 35.61 40.15 44.74 49.07 52.73 55.33 56.54 56.67 56.62

0.8 13.67 15.60 17.32 19.14 21.35 24.21 27.71 31.71 36.06 40.61 45.19 49.47 53.05 55.52 56.59 56.65 56.62

0.9 13.89 15.78 17.49 19.33 21.59 24.52 28.09 32.13 36.50 41.07 45.65 49.88 53.37 55.70 56.64 56.63 56.62

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-16

STANDARD DEVIATION VALUES FOR WEIGHT IN GIRLS (For calculation of SDS scores) Age 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

0 1.28 1.70 2.07 2.45 2.95 3.64 4.59 5.72 6.93 8.13 9.21 10.08 10.74 11.18 11.42 11.46 11.31

0.1 1.33 1.74 2.11 2.49 3.01 3.73 4.70 5.84 7.05 8.24 9.30 10.15 10.79 11.21 11.43 11.45 11.31

0.2 1.37 1.78 2.14 2.54 3.07 3.82 4.81 5.96 7.17 8.35 9.39 19.22 10.84 11.24 11.44 11.44 11.31

0.3 1.42 1.81 2.18 2.59 3.14 3.91 4.92 6.08 7.29 8.47 9.49 10.29 10.88 11.27 11.45 11.43 11.31

0.4 1.46 1.85 2.21 2.63 3.19 4.00 5.03 6.20 7.42 8.58 9.58 10.36 10.93 11.30 11.46 11.42 11.31

0.5 1.51 1.89 2.25 2.68 3.26 4.09 5.14 6.32 7.54 8.69 9.67 10.43 10.98 11.33 11.47 11.41 11.31

0.6 1.55 1.93 2.29 2.73 3.33 4.19 5.26 6.44 7.66 8.79 9.75 10.49 11.02 11.35 11.47 11.39 11.31

0.7 1.59 1.96 2.33 2.79 3.41 4.29 5.37 6.56 7.78 8.89 9.83 10.55 11.06 11.37 11.47 11.37 11.31

0.8 1.62 1.99 2.37 2.84 3.49 4.39 5.49 6.69 7.89 9.00 9.92 10.62 11.10 11.38 11.46 11.35 11.31

0.9 1.66 2.03 2.41 2.89 3.56 4.49 5.60 6.81 8.01 9.11 9.99 10.68 11.14 11.40 11.46 11.33 11.31

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-17

PEDIATRIC LABORATORY VALUES THAT ARE DIFFERENT FROM ADULT VALUES A number of laboratory values differ between children and adults. Of the chemistries commonly monitored in CKD disease, the following have different normal ranges for pediatrics. These are general, normal ranges, not considering the level of kidney function or mode of treatment. Lab Test Serum Albumin g/dL Alkaline Phosphatase ImU/mL Blood Urea Nitrogen mg/dL Serum Cholesterol mg/dL Serum Creatinine mg/dL CO2 Ferritin ng/mL

Newborn 3.5-5.4

Glucose mg/dL Hematocrit %

40-90 44-64

Hemoglobin g/dL

14-24

Iron µmol/L Mean Corpuscular Volume Phosphorus mg/dL

100-250 96-108 4.8-7.4

3-12 53-135 0.3-1.2 ≥ 22 25-200

Infant 4.4-5.4 85-235 (<2) 5-18 70-175 0.2-0.4 ≥ 22 200-600 (1 mo) 50-200 (2-5 mo) 60-100 (< 2 yrs) 39-59 (2-8 wks) 35-50 (2-6 mo) 10-17 (2-6 mo) 9.5-14 (6 mo-1 yr) 80-95

Child 4-5.9 65-210 (2-8) 5-18 120-200 0.3-0.7 ≥ 22 7-142

Adolescent 60-300 (9-15)

0.5-1.0 ≥ 22

70-105 (>2-adult) 30-40 (1-6 yrs)

32-44 (6-18 yrs)

9.5-14 (1-6 yrs)

10-15.5 (6-18 yrs)

50-120 80-95 4.5-6.5

80-95

Reference: Pagana KD, Pagana TJ: Mosby’s Diagnostic and Laboratory Test Reference, 4th Ed.1999 Portale A: Blood Calcium, phosphorus, and magnesium. In Favus M (Ed) Primer on Metabolic Bone Diseases and Disorders of Mineral Metabolism, Lippencott, Williams and Wilkins, 1999. pp 115-118.

11-18

ESTIMATING CALORIE AND FLUID NEEDS OF PEDIATRIC CKD PATIENTS Holliday-Segar Method or Fluid Method This is a quick, simple formula that estimates maintenance calorie needs from weight alone. It assumes that for each 100 calories metabolized, 100 cc of water will be required. This method is not suitable for neonates less than 14 days old, or in conditions associated with abnormal losses. Calories/kg 1st 10 kg body weight 2nd 10 kg body weight Each additional kg

100 50 20

Water (cc/kg) 100 50 20

Example: 15 kg child will need: 1250 cc fluids per 24 hr (83 cc/kg/day) 1250 calories per 24 hr (83 kcal/kg/day) Adapted: Johnson KB, Ed: The Harriet Lane Handbook, 14th Ed., St. Louis, Mosby-Year Book, 1996

11-19

GUIDELINES FOR CHOOSING AN INFANT FORMULA 1. 2. 3. 4. 5. 6. 7.

Infants (12-24 months or less) may require a formula with lower electrolyte levels (especially potassium and phosphorus) than found in standard milk or soy-based infant formulas. Commonly suggested formulas include: Enfamil® (Mead Johnson), Similac® and PM 60/40 (Ross Laboratories), and Good Start® (Carnation). Formulas containing iron are generally required. Infants on peritoneal dialysis may need sodium supplementation to replace dialysis losses. Calories can be concentrated above 20 kcal/oz by adding modular components such as glucose-polymers, sugar, MCT oil, or vegetable oil. Protein can be supplemented with modular protein powders, as needed. Pediatric and adult enteral formulas (such as Pediasure® or Nepro®, Ross Laboratories) may be considered in children over 12 months of age.

11-20

PEDIATRIC FORMULAS USED IN CKD (Composition per 100 mL) Similac® kcal Carbohydrate (gm) Protein (gm) Fat (gm) Sodium (mg/mEq) Potassium (mg/mEq) Phosphorus (mg) Calcium (mg/mEq) Magnesium (mg) Osmolality (mOsm/kg H2O)

67.6 7.2 1.45 3.7 18.3/0.8 71/1.8 38 49/2.5 4.1 300

PM 60/40® 67.6 6.9 1.5 3.77 15.6/0.68 58/1.49 29.3 75.6/3.78 4.06 280

Enfamil® 67.6 7.4 1.42 3.6 18.3/0.8 73/1.9 36 52.7/2.6 5.4 300

Good Start® 67.6 7.4 1.62 3.5 16.2/0.7 66.2/1.7 24.3 43.3/2.2 4.5 265

Pediasure® 100 11.0 3.0 5.0 38/1.7 131/3.4 80 97/4.9 20 365

Reference: Composition of Feedings for Infants and Young Children, Ross Ready Reference, 1996

AVERAGE NUMBER AND VOLUME OF FEEDINGS (INFANT WITHOUT CKD) Age Birth - 1 week 1 week - 1 month 1 - 3 months 3 - 6 months 6 - 9 months 10 - 12 months

Number 6 - 10 7-8 5-7 4-5 3-4 3

Volume 1 - 3 oz (30 - 90 cc) 2 - 4 oz (60 - 120 cc) 4 - 6 oz (120 - 180 cc) 6 - 7 oz (180 - 210 cc) 7 - 8 oz (210 - 240 cc) 7 - 8 oz (210 - 240 cc)

Adapted: Queen PM, Lang CE: Handbook of Pediatrics, ASPEN Publishers, 1993 11-21

NUTRIENT RECOMMENDATIONS FOR PEDIATRIC ACUTE KIDNEY FAILURE (Not dialyzed) Nutrient Protein* HBV Energy Sodium Potassium Phosphorus Calcium Fluid Vits/Mins

Infant Toddler Child (0-1 year) (1-3 years) (4-10 years) 1-2 gm/kg 1.5-1.8 gm/kg 1.0-1.5 gm/kg 50 - 65% 50 - 65% 50 - 65% Use Holliday-Segar or Fluid Method (pg 11-19)

Adolescent (11-18 years) .8-1.0 gm/kg 50 - 65%

Allowances vary considerably. All levels should be monitored closely and recommendations adjusted as warranted.

Assume fluid restriction. Consult with medical team to determine what portion of total fluid allowance is available for nutrition support. Supplement as necessary.

*Goals should be appropriate to kidney function, stage of acute kidney failure, and/or treatment modality.

11-22

NUTRIENT RECOMMENDATIONS FOR PEDIATRIC CKD PATIENTS (Prior to dialysis) Nutrient Energy

Infant 0-0.5 yr: ≥ 108 cal/kg 0.5-1 yr: ≥ 98 kcal/kg

Toddler 102 kcal/kg

Child 4-6 yr: 90 kcal/kg 7-10 yr: 70 kcal/kg

Protein

0-0.5 yr: 2.2 gm/kg 0.5-1 yr: 1.6 gm/kg As tolerated, 1-2 gm/d w/ hypertension (HTN)/edema

1.2 gm/kg

4-6 yr: 1.2 gm/kg 7-10 yr: 1.0 gm/kg As tol, 1-3 gm/day with HTN or edema

Sodium

Potassium Calcium* Phosphorus Fluids Vitamins/ Minerals Trace Mins

Adolescent 11-14 yr: 47 kcal/kg 15-18 yr: 40 kcal/kg 11-14 yr: 55 kcal/kg 15-18 yr: 45 kcal/kg 11-14 yr: 1.0 gm/kg 15-18 yr: 0.9 gm/kg As tol, 3-4 gm/day with HTN or edema

As tol, 13gm/d w/HTN/edema Restriction not usually needed until GFR is below 10% of normal. Most will tolerate ≥ 3 mEq/kg 0-0.5 yr: 400 mg/day 800 mg/day 800 mg/day 1200 mg/day 0.5-1 yr: 600 mg/day Limit P if serum high, low Usually 600-800 mg/day, when serum levels are elevated P formula Unrestricted unless indicated, then replace insensible losses plus urine output. 1 mL MVI drops. * Vit D, Multivitamin or B complex plus C, Vit D, if Multivitamin or B complex plus C. if indicated. indicated by Ca++, PTH, alk phos. Vit D, if indicated Supplement zinc, iron, and/or copper, if needed

* Note: Current practice varies among clinicians regarding the use of standard pediatric multivitamins (MVT) versus B complex plus any renal formulations have higher vitamin levels than recommended for infants. MVT may be appropriate in the infant less than 1 year of age to provide sufficient/appropriate vitamins and minerals for growth and development. Adequacy of vitamin A should be carefully monitored in infants. Reference: Nelson P, Stover J, Eds: Nutrition Recommendations for Infants, Children, and Adolescents with ESRD. A Clinical Guide to Nutrition Care in End Stage Renal Disease, 2nd Ed, ADA, 1994 11-23

NUTRIENT RECOMMENDATIONS FOR PEDIATRIC PATIENTS - HEMODIALYSIS Nutrient Energy kcal/kg K/DOQI RDA for chronological age; monitor response Protein K/DOQI: RDA for chronological age + 0.4 gm/kg Sodium

Infant 0-0.5 yr: ≥108 cal/kg 0.5-1 yr: ≥98 kcal/kg

Toddler 102 kcal/kg

Child 4-6 yr: 90 kcal/kg 7-10 yr: 70 kcal/kg

Adolescent 11-14 yr: % 55/kg & 47/kg 15-18 yr: % 45/kg & 40/kg 18-21 yr: % 40/kg & 38/kg

0-0.5 yr: 2.6 gm/kg 0.5-1 yr: 2.0 gm/kg

≥1.6 gm/kg

4-6 yr: ≥1.6 gm/kg 7-10 yr: ≥1.4 gm/kg

11-14: %/& 1.4 gm/kg 15-18: % 1.3 & 1.2 gm/kg 19-21: %/& 1.2 gm/kg

As tolerated, 1-2 gm/d w/ HTN/edema

As tol, 1-3 gm/d w/ HTN/edema

As tol, 2-4 gm/day w/ HTN/edema

As tol, 2-4 gm/day with HTN/edema

Potassium

1-3 mEq/kg, if serum levels elevated

Calcium

0-0.5 yr: 400 mg/day 800 mg/day 800 mg/day 1200 mg/day 0.5-1 yr: 600 mg/day If serum level high, Usually 600-800 mg/day, when serum levels are elevated use low P formula Replace urine, Replace insensible losses plus urine output insensible losses, + UF, if possible K/DOQI: 100% of Dietary Reference Intake (DRI) for thiamin, riboflavin, pyridoxine, B12, and folic acid. 100% of Recommended Dietary Allowance for vitamins A, C, E, K, copper, and zinc.

Phosphorus Fluids

Vitamins/ Minerals

Reference: Nelson P, Stover J, Eds: Nutrition Recommendations for Infants, Children, and Adolescents with ESRD. A Clinical Guide to Nutrition Care in End Stage Renal Disease, 2nd Ed, ADA, 1994 NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-24

NUTRIENT RECOMMENDATIONS FOR PEDIATRIC PATIENTS - PERITONEAL DIALYSIS Nutrient Energy kcal/kg Include dialysate calories

Infant 0-0.5 yr: ≥108 cal/kg 0.5-1 yr: ≥98 kcal/kg

Toddler 102 kcal/kg

Protein gm/kg

0-0.5 yr: 2.9-3.0 gm/kg 0.5-1 yr: 2.3-2.4 gm/kg

1.9-2.0 gm/kg

Sodium gm/d

As tol, 1-2 gm/d with HTN/ edema

As tol, 1-3 gm/d with HTN/edema Unrestricted, or 1-3 mEq/kg

Potassium mEq/L

Calcium mg/d Phosphorus mg Fluids cc Vits/Mins Reference:

1-3 mEq/kg, if restriction needed

0-0.5 yr: 400 mg/day 0.5-1 yr: 600 mg/day Low P formula, if serum level high Replace all losses K/DOQI: Same as HD

800 mg/day

Child Adolescent 4-6 yr: 90 11-14 yr: % 55/kg & 47/kg kcal/kg 15-18 yr: % 45/kg & 40/kg 7-10 yr: 70 18-21 yr: % 40/kg & 38/kg kcal/kg 4-6 yr: 1.9-2.0 11-14: %/& 1.7-1.8 gm/kg gm/kg 15-18: %/& 1.4-1.5 gm/kg 7-10 yr: 1.719-21: %/& 1.3 gm/kg 1.8 gm/kg As tol, 2-4 As tol, 3-4 gm/d with HTN/edema gm/d with HTN/edema Generally unrestricted

800 mg/day

1200 mg/day

Usually 600-800 mg/day, when serum levels are elevated. Unrestricted, unless signs of fluid overload

Nelson P, Stover J: Nutrition Recommendations for Infants, Children, and Adolescents with ESRD A Clinical Guide to Nutrition Care in End Stage Renal Disease, 2nd Ed. ADA 1994 NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000 11-25

NUTRIENT RECOMMENDATIONS FOR PEDIATRIC PATIENTS – TRANSPLANT Nutrient Energy (After ideal wt to ht is achieved)

Protein

Sodium

Infant 0-0.5 yr: ≥ ³108 cal/kg 0.5-1 yr: ≥ 98 kcal/kg 3 gm/kg initial, RDA after 3 mo 1-3 gm/day initial

Toddler 102 kcal/kg

Child 4-6 yr: 90 kcal/kg 7-10 yr: 70 kcal/kg

Adolescent % 11-14 yr: 47 kcal/kg 15-18 yr: 40 kcal/kg & 11-14 yr: 55 kcal/kg 15-18 yr: 45 kcal/kg

2-3 gm/kg initial RDA after 3 mo

1.5-2 gm/kg initially, then RDA after 3 mo

1.2-1.5 gm/kg initially, then RDA after 3 mo

1-3 gm/d initial, Not restricted, unless HTN/edema

2-3 gm/day initial, Not restricted unless HTN/edema

2-4 gm/d initial. Not restricted unless HTN/ edema

Potassium

Unrestricted, unless serum levels are high.

Calcium Phosphorus Fluids Vitamins Minerals

No restriction, supplement to RDA levels as necessary. May need very high intakes. Supplement as necessary. No restriction (>1.5 x maintenance) Unrestricted; high intake encouraged. May not be necessary, unless very Generally unnecessary; Vit D as needed. malnourished prior to transplant; Vit D as needed Generally unnecessary; supplement iron and magnesium as needed.

Trace Mins

Reference: Nelson P, Stover J: Nutrition Recommendations for Infants, Children, and Adolescents with ESRD in A Clinical Guide to Nutrition Care in End Stage Renal Disease, 2nd Ed. ADA, 1994 11-26

BONE ABNORMALITIES IN PEDIATRIC PATIENTS WITH CKD: 1. 2. 3. 4. 5.

The incidence of renal osteodystrophy is greater in infants, children, and adolescents due to the high rate of bone turnover in the growing skeleton. Radiographic studies of wrists should be performed annually to determine bone age. The maintenance of normal calcium and phosphorus is critical to bone growth. Renal osteodystrophy significantly contributes to growth retardation. Growing bones are more susceptible to alterations in circulating PTH and Vitamin D. Usual dose of calcitriol: IV = 0.5 - 1.5 µg three times per week ; oral = ≥ 0.25 µg daily.

The dose is dependent on serum calcium, serum phosphorus, alkaline phosphatase, and PTH. Treatment should be started when the serum intact PTH levels are 400-500 pg/mL and the serum calcium levels are between 9.5-10.5 mg/L. Close attention must be given to the development of adynamic bone lesions in patients who have PTH levels below 200 pg/mL. Patients with adynamic bone lesions should be managed with low calcium dialysate and Vitamin D therapy should be withheld. References:

Sanchez C, Salusky IB: The renal bone diseases in children treated with dialysis. Adv in Ren Replacement Ther 3(1):14, 1996

11-27

MALNUTRITION IN PEDIATRIC PATIENTS WITH CKD: 1. 2. 3. 4. 5. 6. 7. 8.

Protein-energy malnutrition is the most prominent nutritional disorder in children with CKD. Mild or moderate under nutrition is also common and is labeled “failure to thrive” (FTT) in younger children. The earlier CKD manifests itself, the more the potential there is for FTT and/or growth retardation. FTT can cause a child to miss developmental milestones including development of feeding skills. A tube feeding (NG or GT) may be necessary if oral intake is insufficient to meet nutrient needs. A variety of formulas can be used depending on the age of the child, level of renal function, and available fluid volume. (See choosing an infant formula, page 11-21). Oral stimulation is important for development. Begin solid food intake within the normal infant progression and 4-6 months of age developmentally. Progress to table foods as tolerated. Supplement solids (purees and table food) with modular components of carbohydrate, protein, and fat as needed to reach recommended levels. Growth hormone can be an important adjunct to nutritional management in treating growth retardation in patients with compromised renal function.

K/DOQI: Consider supplemental nutrition support when a patient is not growing normally or fails to consume recommended levels of calories and/or protein. Oral supplementation is the first choice of therapy, followed by tube feeding. Recombinant Human Growth Hormone (hGH) should be considered for dialysis patients with growth potential when: Height for chronological age is more negative than 2 SD or height velocity for chronological age more than negative 2.0 SDS; shows potential with open epiphyses; there are no other contraindications. Protein/energy deficit, acidosis, hyperphosphatemia, and hyperparathyroidism should be correction prior to hGH therapy.

11-28

GUIDELINES FOR ENTERAL FEEDINGS IN PEDIATRIC PATIENTS WITH CKD 1. 2. 3. 4. 5.

Assume the patient will be on a fluid limit. Keep volume as low as possible. Consider 2 kcal/cc formula if electrolyte levels are tolerated. Dialysis may be required to allow provision of adequate nutrition. Choose formulas that are lower in K+ and P, if possible. Monitor serum levels closely. Infant formulas: Increase calorie density by adding carbohydrate or fat modules, rather than concentrating the formula. Choose low protein formulas (AminAid) for the child older than 1 year who is not being dialyzed. When using low protein formulas, monitor electrolytes closely. Low protein formulas may not contain electrolytes, vitamins, or minerals. These formulas can be given by mouth, but palatability is an issue, especially in children.

11-29

GUIDELINES FOR TUBE FEEDINGS IN PEDIATRIC PATIENTS WITH CKD: 1.

2. 3. 4.

The choice of formula depends on the age, diagnosis, renal replacement therapy, and fluid status. Even 2 kcal/cc formulas can be used in children if the strength, volume and rate of administration are increased gradually. Feedings are usually given at night with a continuous drip over 8-12 hours. Start slowly and advance gradually to total volume. Infants may start with 10-20 cc/hour and advance as tolerated. Daytime bolus feedings may be tolerated. The formula concentration and feedings for infants and young children need to be altered frequently in response to growth and laboratory values.

11-30

GUIDELINES FOR PARENTERAL NUTRITION IN PEDIATRIC PATIENTS WITH CKD 1. 2. 3.

4. 5.

6.

Determine available fluid allowance. Use modality specific energy recommendations plus a factor for current medical condition. Obtain indirect calorimetry measurement if available. Start with a 10% dextrose concentration and advance by 5% daily until the goal is reached. Condense dextrose as appropriate to keep volume low to minimize the need for dialysis. Try to keep the total volume to <2 L/day (even lower in smaller patients). Standard amino acid solutions are generally appropriate. Use modality specific protein levels. Children, age 2 or younger, should receive Trophamine. Monitor albumin/prealbumin. Obtain baseline triglyceride levels. If less than 200 mg/dL, begin 20% lipids at 0.5-1.0 gm/kg over 18 hours daily. Recheck triglycerides 6 hours after completion of the infusion. If less than 250 mg/dL, advance lipids as necessary to reach desired calorie level. Maximum lipid infusion levels are 3-4 gm/kg in children and lipids should not exceed 60% of the total calories. Electrolytes:Sodium - individualize as tolerated/appropriate. Potassium - total should not exceed 50 mEq/L. Magnesium - decrease standard solution of 10 mEq/L by half (5 mEq/L). Phosphorus - reduce standard solution of 7.5 mmol/L by ½ of standard. Do not remove entirely because of the risk for hypophosphatemia. Calcium - individualize to maintain acceptable serum levels. MVI - do not add, replace with 1 cc/day of B-complex plus C. Selenium - renal requirements not clear, limit use. Suggest removing after one week on TPN. Acetate, Chloride - individualize to maintain acid/base balance. Zinc, Copper - standard solutions are generally acceptable.

11-31

GUIDELINES FOR UREA KINETIC MODELING IN PEDIATRIC HD PATIENTS: In theory, urea kinetic modeling (UKM) concepts are the same for children as they are for adults. UKM can provide a basis for ongoing assessment of dialysis adequacy and protein nutrition. However, the dynamic metabolic activity in children requires that we recognize special considerations for interpretation and application of urea kinetic calculations. 1. There are much greater variations in body size (10 kg to 100 kg). 2. Growth factor and metabolic requirements are constantly changing especially in the growing child requiring at least monthly UKM assessments. Growing children should be in positive nitrogen balance and in an anabolic state (PNA < dietary protein intake). 3. Total body water is relatively larger in small children (greater volume to weight ratio). 4. The ratio of total body water to weight (volume:weight) can vary as much as 20%, from 0.50 to 0.70, but should be constant for an individual child. 5. Pediatric patients commonly have a relatively greater interdialytic (ID) weight gain, requiring relatively greater ultrafiltration (UF). 6. Individualized target PNAs and urea generation rates are needed because of the varied composition of the diets. (Infant formulas are fairly consistent, toddlers pick at eating, and adolescents may skip meals or eat fast foods). K/DOQI: PNA not well tested in pediatrics. 7. Double pool kinetics may be more accurate in children because of their low absolute TBW and relatively high clearances. 8. Suggest PCR targets: Infant/toddler - ≥1.4 Children - 1.2 to 1.4 Adolescents - ≥1.2 9. Target Kt/V = ≥1.4 (K/DOQI Recommendation: Prescribed Kt/V ≥1.3; Delivered ≥1.2) 10. Other recommendations of frequency/method of measurement, blood draw procedures, and problem solving are the same as for adult HD patients. Most recommendations are based on opinion or adult research. 11-32

GUIDELINES FOR ADEQUACY TESTING IN PEDIATRIC PD PATIENTS Literature is scant and controversial. Most recommendations are extrapolated from adult data. Special considerations for interpretation and application of urea kinetic calculations in pediatric PD patients include: 1. Recommended dwell volumes are relatively greater in children. The surface area of the peritoneal membrane is larger in children than in adults as related to body weight. 2. Dwell volumes of >900 mL/m2 (body size) are recommended for all ages and sizes. 3. In children, CCPD may be more commonly used than CAPD, but this varies from center to center. 4. Initial goals of measured Kt/V and creatinine clearance parallel adult goals. 5. Dietary protein intake must be greater than total protein nitrogen appearance because positive nitrogen balance is essential for a growing child. 6. PET reference curves for children and evaluations of their application are currently being investigated. 7. K/DOQI Recommendations: Adults and Children: CAPD: Kt/V 2.0 CrCl: 60 L/week (high/high average transporters) 50 L/week (low/low average transporters) CCPD: Kt/V 2.1 CrCl: 60 L/week NIPD: Kt/V 2.2 CrCl: 66 L/week References:

Schleifer CR, et al: The Application of UKM to Peritoneal Dialysis: A review of Methodology and Outcome. J Ren Nutr 3:2-9, 1993 Kohaut EC: A Simplistic Approach to Kinetic Modeling. Sems Dial 7:398, 1994 Warady BA: The Use of the PET to Modify PD Modality in Children, Sems Dial 7:403, 1994 Harmon WE: Kinetic Modeling of HD in Children. Sems Dial 7:392, 1994 Buur T, et al: Reliability of HD UKM in Children. Pediatr Nephrol 8:574, 1994 NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 37(1) Suppl , June, 2001

11-33

CALCIUM UROLITHIASIS See notation in Chapter 8, page 8-20.

HYPEROXALURIA See notation in Chapter 8, page 8-22.

PEDIATRIC REFERENCES: Barone M, Ed: The Harriet Lane Handbook, 14th Edition, Mosby-Year Book, St. Louis, 1996 Daugirdas J, Ing TS: Handbook of Dialysis, 2nd Edition, Little Brown, & Co., Boston/NY/Toronto/London, 1994 Fine R, et al: Extended recombinant human growth hormone treatment after renal transplantation in children. JASN 12 (Supp3):S274, 1992 Fine R, et al: Five years experience with recombinant human growth hormone treatment in children with CRF. J of Pediatr Endocrinology 2(1), 1994 Hendricks KM, Walker WA, Eds: Manual of Pediatric Nutrition, BC Decker, Inc., 1990 Holliday MA, et al, Eds: Pediatric Nephrology, 2nd Edition, Williams and Wilkins, 1987 Massie M, et al: Nutritional assessment of children with chronic renal insufficiency. JRN 2(1):2, 1992 Merenstein GB, et al, Eds: Handbook of Pediatrics, 17th Edition, Appleton and Lange, 1994 Queen PM, Lang CE. Eds: Handbook of Pediatric Nutrition, Aspen Publishers, 1993 Sanchez C, Salusky IB: The renal bone diseases in children treated with dialysis. Adv Ren Replace Ther 3(1):14, 1996 Spinozzi N, Nelson P: Nutrition Support in the Newborn Intensive Care Unit, JRN 6(4):188, 1996 Tonshoff B, Fine RN: Recombinant human growth hormone for children with RF. Adv Ren Replace Ther 3(1):37, 1996

11-34

Chapter 2: LABORATORY VALUES/ DRUG NUTRIENT INTERACTIONS

GENERAL INFORMATION The information in this chapter may help identify problems with nutritional significance in CKD patients, but it is not meant to be all inclusive. Some of the signs or symptoms may be present only in the most severe cases. Furthermore, signs or symptoms may also differ based on the type and stage of kidney disease or the modality of treatment. Critical judgment and collaboration with the CKD care team should be used to assess the cause(s) of abnormal laboratory values. Patient laboratory values will depend also on the analytical method and procedure used by the individual laboratory. Results can be influenced by a number of factors and must be interpreted in conjunction with clinical assessment. Reference ranges included in this chapter are as reported in the sources below. There may be minor differences in normal ranges for the elderly and pediatric patients in some laboratory values. The “CKD ranges” are values that may be seen in CKD patients, but may not reflect the desired range. Where available, K/DOQI values are noted. Target ranges vary from clinic to clinic and patient values should be assessed accordingly. A column labeled “Your Lab” has been provided for notation of laboratory or facility-specific normal ranges. The information provided on drug-nutrient interactions is very general. The effects of specific medications can differ from patient to patient. The information is meant to provide a cross reference to patient symptoms. More detailed information can be obtained from specific drug-nutrient interaction resources, and/or a clinical pharmacist with expertise in renal pharmacology. Note: Reference ranges, SI units, and the significance of abnormal values were updated with Mosby’s Diagnostic and Laboratory Test Reference, 4th edition by Pagana and Pagana, 1999, and Clinical Laboratory and Diagnostic Tests: Significance and Nursing Implications by Kathleen Treseler, Appleton & Lange, 1995. Where the information was different from the previous edition of the Pocket Guide, the newest reference was utilized. 2-2

CONVERSION FORMULAS mg to mEq or mEq to mg mEq = mg x valence atomic weight mEq x atomic weight mg = valence

Calcium Chloride Iron Magnesium Phosphorus Potassium Sodium

Symbol Ca++ ClFe++ Mg++ P K+ Na+

“Traditional” to Systeme International (SI) Units Traditional X Conversion Factor = SI

Atomic Wt 40 35 56 24 31 39 23

Valence 2 1 2 2 2 1 1

Albumin BUN Calcium Chloride Cholesterol Creatinine Ferritin Glucose Iron Magnesium Phosphate Potassium Sodium Total Pro

Traditional g/dL mg/dL mg/dL mEq/L mg/dL mg/dL ng/mL mg/dL µg/dL mEq/L mg/dL mEq/L mEq/L g/dL

Factor 10 0.3570 0.2495 1.0 0.02586 88.4 1.0 0.0551 0.1791 0.5 0.3229 1.0 1.0 10

SI g/L mmol/L mmol/L mmol/L mmol/L mmol/L µg/L mmol/L µmol/L mmol/L mmol/L mmol/L mmol/L g/L

Reference: Hunt K: SI Unit Conversion. J Ren Nutr 3(3):146-147, 1993 2-3

LABORATORY TESTS Test

CKD Range

Significance of Abnormal

3.5 - 5.0 g/dL SI units: 35 - 50 g/L

WNL for the laboratory or >4.0 ideal for CKD (K/DOQI)

High: severe dehydration, albumin infusion Low: fluid overload, chronic liver or pancreatic disease, steatorrhea, nephrotic syndrome, protein-energy malnutrition, inflammatory GI disease, infection

Alkaline Phosphatase

30 - 85 IU/L SI Units: 42 - 128 U/L

WNL

Ammonia Levels

15 - 110 µg/dL

WNL

High: renal osteodystrophy, healing of fractures, malignancies Low: congenital hypophosphatemia, possibly in kwashiorkor, general debility, anemia, nephrotic syndrome High: primary hepatocellular disease, Reye’s syndrome, portal HTN, GI bleeding/obstruction w/mild liver disease Low: essential or malignant hypertension

Albumin

Ref. Range

SI Units: 47 - 65 µmol/L

Your Lab

LABORATORY TESTS (CONT.) Test B12

Ref. Range 100-700 pg/mL

Your Lab

CKD Range WNL

Significance of Abnormal High: leukemia, polycythemia vera, severe liver dysfunction Low: pernicious anemia, atrophic gastritis, malabsorption syndrome, inflammatory bowel disease, Zollinger-Ellison syndrome, achlorhydria, pregnancy, vitamin C or folic acid deficiency

60-80 mg/dL (anuric, well dialyzed, and eating adequate protein)

High: w/excessive protein intake, GI bleeding, dehydration, hypercatabolism, CHF (a ↓ in cardiac output causes a ↓ GFR), transplant rejection, inadequate dialysis Low: hepatic failure, over-hydration, acute low protein intake, malabsorption, ↑ secretion of anabolic hormones

SI Units: 74-517 pmol/L

Blood Urea Nitrogen (BUN)

10 - 20 mg/dL SI Units: 3.6 - 7.1 mmol/L

2-5

LABORATORY TESTS (CONT.) Test Serum Calcium*

Ref. Range 9.0 - 10.5 mg/dL

Your Lab

CKD Range WNL (low end) < 9.5 mg/dL

SI Units: 2.25-2.75 mmol/L

*Adjust for low albumin see formula page 8-16

Ceruloplasmin (Cp)

23-43 mg/dL

WNL

Significance of Abnormal High: excess vit D/calcium, ↑ GI absorption, osteolytic disease, carcinoma, excessive vit A, immobilization, primary hyperparathyroidism, aluminum bone disease, dehydration, prolonged use of tourniquet Low: insufficient Vitamin D, malabsorption, during bone building, post-parathyroidectomy, long term Dilantin therapy, hypoparathyroidism with low albumin (lack of carrier), but ionized is usually WNL High: acute inflammatory response cancer, biliary cirrhosis, pregnancy, copper intoxication Low: Nephrotic Syndrome, kwashiorkor, sprue, hyperalimentation, infants

2-6

LABORATORY TESTS (CONT.) Test Chloride

Carbon Dioxide (Total)

Ref. Range 100 - 106 mEq/L SI Units: 98 - 106 mmol/L

Your Lab

23 - 30 mEq/L SI Units: 23 - 30 mmol/L < 200 mg/dL

Cholesterol SI Units: < 5.2 mmol/L

2-7:

CKD Range WNL

WNL ≥ 22 (K/DOQI)

Significance of Abnormal High: excess salt, dehydration (concentration), some forms of metabolic acidosis, excessive use of meds containing chloride, primary hypoparathyroidism Low: diabetic acidosis, K+ deficiency, metabolic alkalosis, excessive sweating, starvation, GI losses (vomiting), chronic pyelonephritis, dilution due to fluid excess, serum chloride is affected by the same conditions that affect serum sodium and moves in the same direction as sodium High: metabolic acidosis Low: metabolic alkalosis

WNL < 150-180 mg/dL Evaluate for nutrient deficit (K/DOQI)

High: high cholesterol/saturated fat diet, hereditary disorders of lipid metabolism, nephrotic syndrome, glucocorticoid therapy Low: acute infection, starvation, protein-energy malnutrition 2-7

LABORATORY TESTS (CONT.) Test Creatinine

Ref. Range 0.5-1.1 mg/dL (F) 0.6-1.2 mg/dL (M)

Your Lab

CKD Range 2-15 mg/dL

Significance of Abnormal High: muscle damage, catabolism, MI, muscular dystrophy, ARF/CKD, use of cephalothin/cimetidine, excessive protein intake, inadequate dialysis, transplant rejection, relates to muscle mass, muscle turnover, and GFR Low: in chronic dialysis <10 may indicate P-E malnutrition and wasting of muscle

WNL

High: arthritis, Crohn’s disease, lupus erythematous, tissue infarction or damage, acute MI, kidney or bone marrow transplant rejection, soft tissue trauma, bacterial infection, postoperative wound infection, UTI, TB, malignant disease

WNL

High: cystic fibrosis, malabsorption, short-gut syndrome, maldigestion due to obstruction of pancreatic or biliary tree, pancreatic insufficiency or fibrosis

SI Units: 44-97 µmol/L (F) 53-106 µmol/L (M)

CReactive Protein

<0.8 mg/dL

Fecal Fat

<5 gm/24 hr

SI Units: NA

SI Units: NA

2-8

LABORATORY TESTS (CONT.) Test Ferritin

Folic Acid

Ref. Range 12 – 300 ng/mL (M) 10 - 150 ng/mL (F)

Your Lab

SI Units: 12 - 300 µg/L (M) 10 - 150 µg/L (F) 5-20 µg/mL

CKD Range ≥100 ng/mL but no known benefit with >800 (K/DOQI)

Significance of Abnormal High: iron overload, many transfusions, dehydration, can be altered in inflammatory state, falsely elevated in active liver disease Low: iron deficiency

WNL

High: pernicious anemia, vegetarianism, recent massive blood transfusion Low: folic acid deficiency, hemolytic anemia, malnutrition, malabsorption syndrome, malignancy, liver disease, pregnancy, alcoholism, anorexia nervosa High: infection, liver disease, leukemia, hyperlipidemia Low: malnutrition

SI Units: 14-34 mmol/L

Globulin

2.3 - 3.4 g/dL

WNL

SI Units: 23 - 35 g/L

2-9

LABORATORY TESTS (CONT.) Test Glucose (Fasting)

Hematocrit

Ref. Range 70 - 105 mg/dL

Your Lab

CKD Range WNL

SI Units: 3.9 - 5.8 mmol/L

<200 non-fasting before dialysis; influenced by dietary intake

42 - 52 % (M) 37 - 47 % (F) SI Units: 0.42-0.52 (M) 0.37-0.47 (F) volume fraction

33 - 36% (K/DOQI)

Significance of Abnormal High: DM, chronic hepatic dysfunction, hyperthyroidism, malignancy, acute stress, emotional distress, burns, diabetic acidosis, pancreatic insufficiency, glucose intolerance Low: hyperinsulinemia, ETOH abuse, pancreatic tumors, liver failure, pituitary dysfunction, malnutrition, extreme exercise High: polycythemia, dehydration Low: anemias, blood loss (endogenous & dialysis), CKD, insufficient EPO

2-10

LABORATORY TESTS (CONT.) Test Hemoglobin

Hemoglobin Alc (Glycosolated hemoglobin GHb, GHB)

Ref. Range 14 - 18g/dL (M) 12 - 16g/dL (F)

Your Lab

SI Units: mmol/L 8.7-11.2 (M) 7.4-9.9 (F) Adult: 4 - 8% “Good” control <7% “Fair” control 10%

CKD Range Variable 11-12 g/dL (K/DOQI)

Significance of Abnormal High: dehydration Low: over-hydration, prolonged iron deficiency, anemias, blood loss, CRF

WNL

High: newly diagnosed/poorly controlled DM, splenectomy, pregnancy, non-diabetic hyperglycemia Low: hemolytic anemia, chronic blood loss, early CKD

SI Units: NA

2-11

LABORATORY TESTS (CONT.) Test Iron

Ref. Range 60-175 µg/dL (M) 50-170 µg/dL (F)

Your Lab

CKD Range WNL

SI Units: 13-31 µmol/L

Lipoproteins

HDL:>45 mg/dL (M) >55 mg/dL (F) LDL: 60-180 mg/dL VLDL: 25-50 mg/dL SI Units: mmol/L HDL: >0.75 mmol/L (M) >0.91 mmol/L (F) LDL: <3.37 mmol/L VLDL: NA

WNL

Significance of Abnormal High: Fe overload, sideroblastic anemias, estrogen/oral contraceptives, hemolysis, ↑ for 1-2 wks after IV iron-dose dependent Low: iron deficiency, low iron intake, long term blood loss, during rapid growth. Diurnal/day-to-day variations are common, but minimized if sample taken w/in same time frame. Varies by lipid fraction that is elevated/low. High: HDL (familial lipoproteinemia, excessive exercise) LDL/VLDL (familial lipoproteinemias, nephrotic syndrome, hypothyroidism, chronic liver disease, poor glycemic control) Low: HDL (familial hypoliproteinemia, hepatocellular disease, hypoproteinemia from malnutrition or nephrotic syndrome) LDL/VLDL (familial hypolipoproteinemia, hypoproteinemia from malabsorption, severe burn or malnutrition) 2-12

LABORATORY TESTS (CONT.) Test

Ref. Range

Lymphocyte Count (total = % lymphocytes x WBC) Magnesium

1500 - 4000 mm3

Your Lab

CKD Range WNL

SI Units: NA Investigate <1200 - 1500 WNL

1.2 – 2.0 mEq/L SI Units: 0.6-1.0 mmol/L

Mean Corpuscular Volume (MCV)

80 - 95 µm3

WNL

SI Units: NA

Significance of Abnormal High: acute viral infections, collagen disease, hyperthyroidism, high altitude Low: malnutrition (synthesis requires adequate calories/protein), adds power to significance of ↓ albumin, stress High: w/excess intake of Mg+ in water, dialysate, Mg+ containing parenteral infusion or OTC medications, dehydration Low: w/some diuretics, ketoacidosis, hypercalcemia, ETOH abuse, refeeding syndrome, diarrhea/malabsorption, malnutrition High: folic acid/B12 deficiency, cirrhosis, reticulocytosis, chronic alcoholism Low: chronic iron deficiency, anemia of chronic disease (MCV levels indicative of anemias: pernicious >120; microcytic <78; often seen with iron deficiency <64)

2-13

LABORATORY TESTS (CONT.) Test Phosphorus

Ref. Range 3.0 - 4.5 mg/dL

Your Lab

CKD Range 3.5 - 6.0 mg/dL

SI Units: 0.97 - 1.45 mmol/L

Potassium

3.5 – 5.0 mEq/L SI Units: 3.5 - 5.0 mmol/L

3.5 - 6.0 mEq/L

Significance of Abnormal High: CKD, osteodystrophy, vit D intoxication, diurnal rhythm-evening or afternoon as much as 2x the am level, excessive intake, inadequate P binder Low: vit D deficiency, low intake, excess P binding, malabsorption/diarrhea/vomiting, alkalosis, diabetic acidosis, diuretic therapy, alcoholism, refeeding syndrome, post parathyroidectomy, osteomalacia High: CKD, tissue destruction, shock, acidosis, dehydration, hyperglycemia, aldosterone antagonistic overuse, diuretics, falsely ↑ w/tourniquet, excessive oral intake, inadequate dialysis, or inappropriate dialysate K+, compression/fist clenching prior to sample Low: diuretic therapy, ETOH abuse, stress response, vomiting/diarrhea/laxative or enema abuse, malabsorption, correction of diabetic acidosis

2-14

LABORATORY TESTS (CONT.) Test Prealbumin/ Transthyretin

Ref. Range 15 – 36 mg/dL

Your Lab

Significance of Abnormal High: administration of corticoids Low: neonate, liver disease, malnutrition, inflammation

≥30 mg/dL (K/DOQI)

SI Units: 150 - 360 mg/L

Protein, Total

CKD Range

6.4 – 8.3 g/dL

WNL

SI Units: 64 - 83 g/L

Intact Parathyroid Hormone (iPTH)

Intact: 10 - 65 pg/mL

150 – 300 pg/mL (Target for iPTH)

N terminal: 8 - 24 pg/mL C terminal: 50 - 330 pg/mL

High: dehydration, acute/chronic infectious disease, leukemia/multiple myeloma Low: malnutrition, malabsorption, cirrhosis, steatorrhea, edema, nephrotic syndrome High: hyperparathyroidism, nonPTH producing tumors, lung or kidney cancer, hypocalcemia, malabsorption syndrome, vitamin D deficiency, rickets Low: hypoparathyroidism, hypercalcemia, metastatic bone tumor, sarcoidosis, vitamin D intoxication, hypomagnesemia

SI Units: NA Editorial Note: Reference and appropriate CKD ranges for 3rd generation PTH are currently being determined. Variance between third and second generation iPTH depends on the patient-specific level of PTH fragment (7-84) that is measured by the second generation iPTH. Concurrent measures of 2nd and 3rd generation iPTH may be helpful, especially where previous (second generation) values and the clinical picture are inconsistent with current (third generation) PTH measurements. In research done at Satellite Laboratory Services, Redwood City, CA, (368 patients), the 3rd generation PTH values were from 0.47 to 0.53 lower than 2nd generation PTH values in most (97-98%) patients. 2-15

LABORATORY TESTS (CONT.) Test Reticulocyte Count

Ref. Range 0.5% - 2%

Your Lab

CKD Range Variable in response to EPO

Significance of Abnormal Index of bone marrow activity; reflects early change in RBC production High: hemolytic anemia, acute bleed Low: certain anemias due to ineffective erythropoiesis (defic. of iron, B12, folic acid, B6) or anemia of chronic disease

RBC Count Multiply automatic counter values X 1 million for total #)

million/mm3 4.7 - 6.1 (M) 4.2 - 5.4 (F)

Sodium

136-145 mEq/L

WNL

SI Units: NA

SI Units: 136-145 mmol/L

WNL

High: high altitude, temporarily w/strong emotion, diurnally, cold shower, reduced plasma volume, dehydration Low: anemia, hemorrhage, infectious disease, iron deficiency High: dehydration, diabetes insipidus, often masked by water retention Low: over hydration, inappropriate ADH diuretic use, burns, starvation, adrenal insufficiency, nephritis, hyperglycemia, diabetic acidosis, hyperproteinemia 2-16

LABORATORY TESTS (CONT.) Test TIBC Transferrin = (0.8 x TIBC)-43

Ref. Range 250-420 µg/dL

Transferrin

Adult: mg/dL 215-365 (M) 250-380 (F)

Transferrin Saturation

Your Lab

SI Units: 45-73 µmol/L

CKD Range WNL Varies with iron stores

WNL

SI Units: NA 20 - 50% (M) 15 - 50% (F)

≥20% but no benefit to >50% (K/DOQI)

SI Units: NA

Triglycerides

WNL < 200 mg/dL

40-160 mg/dL (M) 35-135 mg/dL (F) SI Units: 0.45-1.81 mmol/L 0.40-1.52 mmol/L

Significance of Abnormal High: chronic iron deficiency, pregnancy, alcoholism, acute hepatitis Low: cirrhosis, malnutrition, collagen or chronic disease/infection, iron overload, inflammation High: chronic iron deficiency, pregnancy, alcoholism, acute hepatitis Low: cirrhosis, malnutrition, collagen or chronic disease/infection, iron overload,inflammation High: iron overload, pregnancy, alcoholism, acute hepatitis Low: cirrhosis, malnutrition, collagen or chronic disease/infection, iron deficiency

High: liver disease, gout, pancreatitis, ETOH abuse, MI, diabetes, PD, use of steroids, nephrotic syndrome Low: malnutrition, malabsorption

2-17

LABORATORY TESTS (CONCLUSION.) Test Uric Acid

WBC Count

Zinc

Ref. Range 2.1-8.5 mg/dL (M) 2.0-6.6 mg/dL (F) SI Units: (mmol/L) 0.15 - 0.48 (M) 0.09 - 0.36 (F) 5000–10,000 mm3 SI Units: 5-10 x 109/L

85 - 120 µg/dL

Your Lab

CKD Range WNL

Significance of Abnormal High: gout, early CKD, thiazide diuretics, starvation Low: with high salicylate doses, hepatic failure

WNL

High: leukemic neoplasia, acute infection or inflammation, fever, anemia, tissue necrosis, trauma, stress Low: radiation, chemotherapy, bone marrow failure, dietary deficiencies, overwhelming infection, autoimmune diseases High: contaminated sample, hemolysis Low: low intake or absorption / increased loss or needs, alcoholism, cirrhosis of the liver

WNL

References: Pagana KD, Pagana TJ: Mosby’s Diagnostic and Laboratory Test Reference,1999 Treseler, K: Clinical Laboratory and Diagnostic Tests, Appleton & Lange, 1995 Ravel R: Clinical Laboratory Medicine. Yearbook Medical Publishers, 1984

2-18

POSSIBLE NON-DIETARY CAUSES OF HYPERKALEMIA IN KIDNEY DISEASE Mild to moderate renal insufficiency: primary cause is a defect in distal tubular K+ secretion with or without distal renal tubular acidosis. Laboratory error: hemolysis caused by improper blood sampling or specimen handling Acidosis: each 0.1 decrease in arterial pH may increase serum potassium by 0.6 to 1.0 mEq/L High serum glucose: shift between cell and serum Insulin Deficiency: in diabetics Inadequate dialysis: poorly functioning vascular access, too little time, insufficient blood flow, inappropriate dialyzer. Other chemistries are usually elevated in conjunction with potassium Dialysate potassium concentration too high Drug Interactions: K-penicillin, beta blockers, angiotensin-converting enzyme inhibitors, muscle relaxants, non-steroidal anti-inflammatory agents, steroids, cyclosporin, other OTC medications Tissue destruction: rhabdomyolysis, burns Catabolism/starvation: cell breakdown with release of potassium into serum, usually in combination with significant weight loss Concomitant disease: Addison’s disease, sickle cell anemia Decreased gut excretion: severe, long term constipation Adapted: Beto J: Hyperkalemia: Evaluation of Dietary and Non-Dietary Etiology. J Ren Nutr 2:28-29, 1992

2-19

SIGNS AND SYMPTOMS OF ABNORMAL SERUM POTASSIUM System Laboratory Clinical Finding Skeletal/Muscle

Cardiac Effects

GI/Smooth Muscle

Nervous System

Hypokalemia Hyperkalemia < 3.5 mEq/L > 6.0 mEq/L Frequently none until serum potassium levels are very high or low. General muscle weakness, cramps, Usually no symptoms; could have difficult respiration general weakness, tingling, difficult speech, respiration, and ambulation Tachycardia with cardiac Bradycardia, cardiac block or dilation/block/arrest, presence of U waves, arrest, low pulse rate, prolonged flattened T and U waves PR interval, widened QRS, tall Twaves, flattened P-waves Decreased peristalsis, early nausea/ Decreased peristalsis leading to vomiting, constipation, abdominal nausea and diarrhea distention, anorexia Listlessness, lethargy Irritability, mental confusion

References: Tisher C, Wilcox C: Nephrology for the House Officer, Williams & Wilkins, 1993 Treseler K: Clinical Laboratory and Diagnostic Tests, Appleton & Lange, 1995

2-20

ACIDOSIS/ACIDEMIA Acidemia – abnormally increased hydrogen ion concentrations in the blood. Acidosis, metabolic - disturbance where the acid-base status of the body shifts toward the acid side due to changes in the fixed acids and bases in the body. Acidosis refers to the existence of one or more conditions that promote acidemia. Acid production in dialysis patients is a function of the net rate of protein degradation (protein equivalent of total nitrogen appearance) and is estimated to be 0.77 x PNA. The estimated alkali needed per dialysis treatment is 240 mmol and is usually delivered in the dialysate solution, usually as bicarbonate or acetate. While serum bicarbonate levels are often low in maintenance hemodialysis patients, direct plasma pH provides a more absolute confirmation of acidosis or acidemia. There is evidence that acidosis causes loss of lean body mass and may increase protein catabolism. Several studies have shown that metabolic acidosis blocks the ability of CKD patients to adapt to a low protein diet. Others suggest that muscle protein degradation is higher in patients with lower serum bicarbonate levels. Conversely, treatment with NaHCO3 decreases protein degradation. Some studies suggest that acidosis may also cause negative nitrogen balance and inhibit albumin synthesis. While future research may elicit the full clinical impact of acidosis in CKD patients, current recommendations suggest maintaining serum bicarbonate levels at ≥22mEq/L (KDOQI). Supplementation of bicarbonate in dialysate or orally may be needed to maintain acceptable bicarbonate levels throughout the interdialytic period. Dialysate concentrations of >38 mmol/L have been shown to safely increase predialysis serum bicarbonate levels as have oral doses of sodium bicarbonate (usually 2 – 4 g/d or 25 to 50 mEq/d). References:

NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure, Am J Kidney Dis 35 (6) Suppl 2, p S38-S39, June, 2000 Mitch WE: Mechanisms Causing Muscle Wasting in Uremia, J Ren Nutr 6(2):75-78, 1996 Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997

2-21

ACIDOSIS/ALKALOSIS Type Metabolic Acidosis

HCO3 Decreased

Blood pH Decreased

PCO2 Normal

Causes Diarrhea, uncontrolled diabetes or diabetic ketoacidosis, shock, starvation, large chloride infusion, CKD, sepsis or severe infection, excessive protein intake, intestinal fistula Most common cause in dialysis patients is vomiting, reduced protein intake, intensive dialysis

Metabolic Alkalosis

Increased

Increased

Normal

Respiratory Acidosis Respiratory Alkalosis

Normal

Decreased

Increased

Chronic lung disease, depression of ventilation rate

Normal

Increased

Decreased

Hyperventilation (emotions, pain, respirator overventilation) hypoxia

Reference: Daugirdas JT, Ing TS: Handbook of Dialysis, Little, Brown & Co., Boston, 1994 Schrier R (Ed): Manual of Nephrology, Little, Brown, & Co., Boston, 1990 Pagana KD, Pagana TJ: Mosby’s Diagnostic and Laboratory Test Reference, 4th Ed. 1999

2-22

Na+/ K+ CONTENT OF SALT AND SALT SUBSTITUTES (Per ¼ tsp.) Brand Iodized Salt Adolph’s Salt Substitute+ Adolph’s Seasoned Salt-Free+ Durkee’s Low Sodium Salt Substitute+ Durkee’s Seasoned Salt Lite+ Lawry’s Seasoned Salt Free+ Morton Lite Salt Morton Salt Substitute Morton Seasoned Salt Substitute Natures Seasonings (Morton) NoSalt, Seasoned Alternative+ NoSalt Alternative NuSalt Papa Dash Salt Lovers+ Papa Dash Light, Light, Light+ Savorex, Loma Linda+ Sterling Lo-Salt+

Na+mg 590 0 2 0 135 2 280 0 0 380 0.5 0 0 240 90 80 115

K+mg Trace 550 226 480 0 226 350 600 480 tr 333 650 663 tr tr 53 150

References: Pennington, J. Food Values of Portions Commonly Used, 17th Ed, 1998 Product Update, J Ren Nutr 5(2):91-92, 1995 Manufacturers’ Labels + Unable to obtain updated information on these products. 2-23

DRUGS THAT MAY IMPAIR ABSORPTION OR UTILIZATION OF NUTRIENTS Drug-nutrient interactions depend on the drug dose and timing of administration. Multiple drugs may have simultaneous and compounding effects.Phosphate binders/calcium supplements can affect and/or be affected by many drugs and should be taken away from other medications if at all possible. Bicarbonate administration reduces folate and iron absorption. Drug

Alcohol Antibiotics:

Cycloserine Neomycin Isoniazid Tetracycline Tobramycin

Antacids* Anticoagulants Anticonvulsant: Phenobarbital Anti-Gout Anti-inflammatory Corticosteroids Diuretics Hypocholesterolemics Laxatives Mineral Oil

Nutrient

Increased excretion of Mg++, K+ zinc, impaired utilization of folic acid Decreased levels of B12 B6, folic acid Decreased absorption: fat, lactose, protein, vit A, D, K, B12, Ca++, K+, Fe++ Pyridoxine deficiency Ca++, Mg++, iron, zinc Increased urinary loss of K and Mg, Hypokalemia Decreased absorption of Phosphorus, Fe++ Decreased Vitamin K-dependent coagulation factors B12, folic acid, Ca++, Mg++, Pyridoxine, Vitamin K & D Pyridoxine may increase drug effect, Incr excretion of K+, Na+, Ca++, Mg++, P, Mg++, amino acids, Chloride, vit B2 Folic acid, Na+, K+, fat, vit C, nitrogen, B12 Incr protein catabolism/decr synthesis; decr absorption of Ca++, P, K+; incr need for B6, Folate, vits C, D, zinc Incr urinary excretion of Mg++, zinc, K+, thiamin Decr absorption: fat, carotene, vit A, D, K, B12, Fe Increased fecal loss of fat, Ca++, K+, Mg, fluids, most vitamins, carotene, Decr absorp vit A, D, E, K, Ca++ May not be clinically significant.

References: Mosby’s Nursing Drug Reference, Mosby 2000 Moore MC: Nutritional Care 4th Ed. Mosby’s Pocket Guide Series, 2001 Alpers DH, et al: Manual of Nutritional Therapeutics. Lippincot Williams & Wilkins, 2002 2-24

DRUG-NUTRIENT INTERACTIONS Medications can alter absorption or enzyme systems; damage intestinal mucosa/alter normal flora; alter cellular metabolism; or cause excess excretion (urine/stool). They can also cause a myriad of symptoms including diarrhea, N & V constipation, anorexia, GI distress, dry mouth, altered taste, change in appetite, change in GI secretion and/or transit time. In addition, some foods can affect drug actions as indicated below. Diet Factor Caffeine, Sodium restriction Potassium deficiency Grapefruit juice Natural licorice Salt Substitutes Tyramine/dopamine sources: (liver, hard salami, pickled or aged proteins, aged cheese, yogurt, fava beans, raisins, figs, banana, etc)

Drugs Affected Lithium Digitalis Cyclosporin, nifedipine, calcium channel blockers Thiazides ACE inhibitors MAO inhibitors

Actions Increases drug toxicity Decreases first pass extraction and causes increased drug levels Excessive K+ loss, cardiac dysrhythmia Elevation of potassium levels Heachache, hypertensive crisis, potential intracranial hemorrhage

Reference: Moore MC: Nutritional Care. 4th Ed. Mosby’s Pocket Guide Series, 2001

2-25

POTENTIAL NUTRITION EFFECTS OF COMMON IMMUNOSUPPRESSIVE DRUGS Drug Azathioprine - Imuran

Nutrition -related side effects

Basiliximab - Simulect

Nausea, vomiting, stomatitis, esophagitis, pancreatitis, muscle wasting Vomiting, nausea, diarrhea, constipation, abdominal pain

Corticosteroids/Prednisone Deltasone, Liquid prednisone, Meticorten, Orasone Cyclosporin Sandimmune, Neoral

Diarrhea, nausea, abdominal distension, GI hemorrhage, increased appetite, pancreatitis, osteoporosis, poor wound healing, fluid retention, hyperglycemia Nausea, vomiting, diarrhea, oral candida, gum hyperplasia, pancreatitis, hepatoxicity, nephrotoxicity, hyperkalemia

Muromonab-CD3/Orthoclone OKT3 Mycophenolate CellCept Sirolimus - Rapamune Tacrolimus Prograf

Nausea, vomiting, stomatitis, muscle wasting, peripheral edema GI bleeding, abdominal pain, hypophosphatemia, hypercholesterolemia, hyperglycemia Hyperlipidemia N & V, diarrhea, constipation, albuminuria, proteinuria, hematuria, hyper-/hypokalemia, hypomagnesemia, hyperglycemia, nephrotoxicity Diarrhea, gastritis, hyperkalemia

Tymo Globulin (Anti-thymocyte Globulin)

Reference: Skidmore-Roth L: 2000 Mosby’s Nursing Drug Reference, 2000 Kopple JD, Massry S, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997 Simon & Schuster Interactive: The Pill Book on CD-ROM, 1996 2-26

HERBAL SUPPLEMENTS Alternative medical therapies are prevalent in the US, both in generally healthy individuals and in those with various diseases / illnesses. Clinicians must create an environment of openness for CKD patients to report information regarding the use of alternative therapies. In general, use of medicinal herbs can be dangerous and inadvisable for those with CKD. Medical herbs can have potent pharmacological activity, questionable chemical components, microbial contamination, and effects that interfere with conventional medications. In addition, research on efficacy and safety is lacking, especially in CKD. Common categories of herbs are women’s or men’s health, cold/flu, memory/concentration, sleep, cardiac/cholesterol, weight loss, anxiety/depression, and headache. Commonly Used Herbs in the US Herb St. Johns Wart

Use Anxiety/depression

Echinacea

Cold/flu symptom relief

Garlic

Cardiac/reduce lipid levels

Ginseng

Multiple: stress, B/P, depression, memory

Ginko Biloba

Memory, concentration

Valerian

Insomnia

Feverfew

Headaches, migraine

Comments/Effects Interacts with many drugs, including immunosuppressant drugs, hidden K+ Could worsen autoimmune disease/Type I DM, interact w/antirejection drugs Side effects: Bad breath, gastritis, diaphoresis, light headedness, impaired blood clotting, can affect insulin and oral antidiabetics Can create anxiety, increased B/P, insomnia, headaches, asthma attacks, hypoglycemia, decreased anticoagulant activity. Do not use in CKD Headache, anxiety, restlessness, incr risk for bleeding, N & V, diarrhea, anorexia Headache, excitability, uneasiness, cardiac disturbances, N & V, anorexia, hepatotoxicity, insomnia, vision changes, may negate warfarin Mouth ulcers, incr heart rate, limits iron absorb, N & V, anorexia, muscle/joint pain 2-27

CKD AND HERBAL MEDICINES Classification Potentially Beneficial

Herbs Rheum rhaponticum (Chinese rhubarb), Epimedium sagittatum, Man Shen Ling, Rhizome wheat starch, Acacia senegal (Gum Arabic)

Potentially Detrimental

Mixture: (C. Magnolia officinalis, R. stephaia, Tetrandra, R. Aristolochia, Fanchi) Artmisia asbinthium (wormwood plant), Glycyrrhiza glabra (licorice), Chuifong tuokuwan (Black Pearl), Tung sheuh (Cow’s Head Brand)

Reported Effects Improved proteinuria, delayed progression, improved protein status, improved kidney function/edema/anemia, increased diuresis. Polyuria resulting in dehydration, ARF, CKD, and stone formation, potassium imbalance

References: Geraghty ME: Herbal Supplements for Renal Patients: What do we know? NNI, March 2000 Skidmore-Roth L: Mosby’s Handbook of Herbs and Natural Supplements. Mosby, Inc. 2001

2-28

Chapter 3: NUTRIENT CALCULATIONS

GENERAL INFORMATION Nutrient recommendations in this chapter are compiled from a number of sources as noted and reflect the K/DOQI nutrition practice guidelines where available. While the information here is appropriate for a majority of patients, each patient should be assessed individually and thoroughly. Base nutrient recommendations on the findings in the nutrition assessment, clinical expertise, and common sense. Do not restrict the diet above what is necessary to maintain clinical, nutritional, and metabolic status. Editorial Comment: Methods of patient instruction vary widely within renal nutrition practice. Patients should be given written instruction on appropriate food choices based on their level of kidney function, treatment modality, clinical status, and biochemical profile. Instruction should also be appropriate for the patient’s level of education and literacy skills. Providing a written meal pattern or guide serves several purposes. It can prove that a patient has received instruction and written guidance in the event of a medical-nutrition crisis or significantly abnormal laboratory values. Verbal follow-up with the patient can refer the patient back to the previously provided written information. Failure to provide written instruction based on the patient’s individual needs may put the dietitian at risk of legal accountability for an event such as hyperkalemia. With the focus on preventing malnutrition and maintaining or improving the nutrition status of our patients, we have moved toward much more liberal meal plans. Provision of written and verbal nutrition guidance for patients and/or their support persons is of utmost importance. Failure to provide verbal and written guidance is unacceptable renal nutrition practice. The ability to provide quality nutrition care depends on adequate staffing. According to the K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure, “There appears to be a general sense among renal dietitians, based on experience, that an individual dietitian (full time) should be responsible for the care of approximately 100 maintenance dialysis patients, but almost certainly no more than 150.” Other documentation (NKF-CRN Staffing Guidelines, CRN of Northern California/Northern Nevada) suggests that staffing should be based on total number of patients with additional time for higher acuity levels (language barrier, diseases, lack of economic/social resources, advanced age) within the patient population and new patients (usually 80-100 patients per FTE). Those patients with higher acuity levels and new patients require additional intervention and dietitian time over stable MD patients. 3-2

DAILY NUTRIENT RECOMMENDATIONS FOR CKD Acute1 Protein gm/kg3

0.6-0.8 Based on renal function/treatment

Energy kcal/kg3

35-50 depends on stress/status of nutrition

Na+ gm/day

1-2 Based on B/P, edema; replace diuretic phase 2 Maintain serum <5 mEq/L Replace loss diuretic phase

K+ gm/day

1 2

3

Nephrotic Syndrome

CKD

PD

HD

Transplant Post-op 1.3-2.0

Chronic 0.8-1.0

0.8-1.0 Replacing urine loss is controversial

K/DOQI: ≥1.2 ≥ 50% HBV

K/DOQI: ≥ 1.2-1.3 ≥50% HBV

35 unless pt is obese; high complex CHO; low cholesterol; <30% fat

K/DOQI: 30-35 >60 yrs 35 <60 yrs

30-35 Maintain SBW, limit fat to 30% kcal, < 300 mg cholesterol/day

Varies from 1-3 to no added salt

1-2

1-3

K/DOQI: 30-35 >60 yrs 35 <60 yrs including dialysate calories 2-4 Monitor fluid balance

Usually unrestricted unless serum level is high

Usually unrestricted

2-3 Adjust to serum levels

3-4 Adjust to serum levels

Unrestricted, unless serum level high, may need diet restriction with cyclosporin

K/DOQI: GFR <25 mL/min /1.73 m2 0.60-0.75 gm/kg >50% HBV K/DOQI: 30-35 >60 yrs 35 <60 yrs

2-4

2-4

TPN recommendations are in Chapter 9. Editorial Note: A 1 gm Na+ (sodium) restriction on HD or PD is generally difficult to achieve in an outpatient setting and seldom needed with dialysis. Based on standard or adjusted body weight 3-3

DAILY NUTRIENT RECOMMENDATIONS FOR CKD (CONT.) Acute1

CKD

Nephrotic Syndrome

HD

PD

Post-op RDA supplement as needed

Chronic RDA

< 2.0-2.5 Include binder load

0.8-1.5

0.8-1.5

Output plus 1000 cc

Maintain balance

Unrestricted, unless overloaded

C: 60-100 mg B6 - 2 mg Folate - 1 mg B12 – 3 µg/d RDA others Vit E-15 IU/d Zinc-15 mg/d Individualize Fe, Vit D

Same as HD but may need 1.5 to 2 mg of B1 due to dialysis loss

RDA, may need additional Vitamin D

Phosphorus mg/gm pro or mg/day

Maintain serum value WNL

10-12 mg/gm protein or 10 mg/kg/day

≤ 12 mg/kg/day

10-12 mg/gm protein < 900 mg/day adjust for pro

10-12 mg/gm protein or < 900 mg/day, adjust for pro

Calcium gm/day

Maintain serum WNL (adjusted for low albumin) Output plus 500 cc

1.0-1.5 < 2-2.5 incl binder load

Same as predialysis

< 2.0-2.5 Include binder load

No restriction

Maintain balance

RDA: Bcomplex & C; Individualize Vit D, Fe, Zinc

Same as CKD Research needed to quantify needs. May need Vitamin D

Fluid cc/day

Transplant

Vitamins/ Minerals (Daily)

RDA: adjust to degree of catabolism, TPN - may require multivitamin & minerals

Fiber

Increased dietary fiber may be beneficial for CKD patients, however, optimal dose, source, and long term clinical benefits have not yet been established. 20-25 gm/day has been suggested.

References: Kopple JD and Massry SG Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997 rd Mitch WE and Klahr S Eds: Handbook of Nutrition and the Kidney, 3 Ed, Little, Brown & Co., 1998 NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000 3-4

NUTRITION RECOMMENDATIONS FOR CKD PATIENTS NOT ON DIALYSIS Stage 1 2 3 4 5

Description GFR (mL/min/1.73 m2) Kidney damage with normal or increased GFR ≥ 90 Kidney damage with mild decrease in GFR 60-89 Moderate decrease in GFR 30-59 Severe decrease in GFR 15-29 Kidney Failure < 15 (or dialysis)

Individuals with GFR <60 mL/min/1.73 m2 (stages 3, 4, 5) should undergo assessment of dietary protein and energy intake and nutrition status. Status should be monitored at regular intervals. (Nutrition Guidelines 23, 26) Nutrient recommendations (Nutrition Guidelines 24, 25) for individuals with GFR <25 mL/min/1.73 m2: 0.6-0.75 gm protein/kg SBW or ABW and 35 kcal/kg SBW or ABW for those <60 years of age and 30-35 for those >60 years of age. Reference: NKF K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation Classification, and Stratification. Am J Kidney Dis 39 (Suppl 1):S1-266, 2002

3-5

L-CARNITINE SUPPLEMENTATION IN MD PATIENTS Area of Impact Lipid abnormalities Intradialytic complications Patient well-being Muscle/cardiac function Exercise tolerance Protein/muscle metabolism Anemia

Supplement Recommendations:

Potential Benefits Reported by Some Investigators in their Research Findings Results variable Lower incidence of intradialytic hypotension/muscle cramps Patient/staff report significant improvement of patients’ sense of well-being Lower rate of arrhythmia, improved cardiac function, decreased cardiomegaly/cardiomyopathy Reported improvement in muscle function and oxygen consumption Decr serum urea nitrogen/Cr/phosphate due to decr in protein/muscle catabolism; Incr albumin/BW Increased hematocrit/hgb and lower EPO dose, L-carnitine is found in phospholipids that make up the red cell membrane, w/ supplementation the red cell membrane is more stable w/ less cell fragility and longer cell life span; may help clear toxins that hinder erythropoiesis IV dose: 10-20 mg/kg/day Oral Carnitine is not indicated for CKD patients. Maintenance Dose: Undetermined, dialysis losses are significant and ongoing; no known harm

Deficiency is multifactorial: inadequate intake of carnitine-rich foods, lack of kidney production, dialysis removal (70% of serum carnitine is cleared in a 3 hour treatment). Serum carnitine is preserved at the expense of muscle carnitine with the potential of creating significant carnitine deficiency over time in CKD patients treated with dialysis. K/DOQI Clinical Practice Guidelines for Nutrition in CRF note:supplementation of L-carnitine in MD patients may improve subjective symptoms (malaise, muscle weakness, intradialytic cramps, hypotension, quality of life) and be most helpful in the treatment of EPO-resistant anemia. Reference: Brass EP, Adler S, Sietsema E, et al: Intravenous L-Carnitine Increases Plasma Carnitine, Reduces Fatigue, and May Preserve Exercise Capacity in HD Patients. Am J Kidney Dis 37(5):1018-1028, 2001 NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000 Kletzmar J, Mayer G, Legenstein E, et al: Anemia and carnitine supplementation in HD patients. KI 55(Suppl 69):S93-106, 1999 Vesela E, Racek J, Trefil L, et al: Effect of L-Carnitine Supplementation in HD Patients. Nephron 88:218-223, 2001 3-6

NUTRIENT RECOMMENDATIONS FOR THE PREGNANT DIALYSIS PATIENT Nutrient Protein* Calories* Sodium** Potassium Calcium Phosphorus Magnesium Fluid** Fiber Vitamins/ Minerals

Recommendation 1 gm/kg + 20 gm/day Rec. dialysis level + 100-300 kcal Individualize Depends on RRF/serum levels 1000-1600 mg/day Balance of diet/binders As needed to prevent hypomagnesemia Individualize to RRF, BP, hydration Encourage increased dietary fiber Supplement as for dialysis with additional on individual basis plus zinc. Vitamin C <150 mg/day.

Goals Meet increased needs, BUN <45-50 mg/dL Dry weight gain per prenatal normals BP control, euvolemia Serum level: 3.5-5.5 mEq/L Serum level: WNL Serum level: 4.5-5.5 mg/dL Serum level WNL ID gain < 1 kg, minimal fluid shift Prevent constipation Replace losses, meet additional needs, maintain serum ferritin >100 µg/L Other: CO2 WNL, creatinine 5-8 mg/dL

* Based on pre-pregnancy SBW or ABW. ** Hypertension and hypotensive episodes are common and dangerous complications. Increased dialysis (by at least 50%, 5-7 days a week) is recommended to minimize fluid shifts and prevent build up of uremic toxins. Dialysate bicarbonate concentration may need to be decreased to prevent metabolic alkalosis with daily dialysis. References: Levy DP, Giatras I, Jungers P: Pregnancy and end stage renal disease-past experience and new insights. Nephrol Dial Transplant 13:3005-3007, 1998 Wilkens K, Schiro K: Suggested Guidelines for Nutrition Renal Patients. ADA, 1992 Grossman S, et al: Nutrition in the Pregnant Dialysis Patient. J Ren Nutr 3(2):56-66, 1993 Hou S: Pregnancy and birth control in dialysis patients. D & T 23:22-26, 1994 3-7

NUTRIENT RECOMMENDATIONS FOR AIDS Nutrient Protein

AIDS 1.5-2.5 gm/kg actual or usual body weight

Calories

35-45 calories/kg actual or usual BW

Fat

< 30% of kcal/modify type of fat based on fat malabsorption Estimated safe/adequate amount; 1.1-3.3 gm/day Estimated safe/adequate amount; 1.9 -5.6 gm/day May need supplement if diarrhea is present 2 times RDA 2 times RDA No restriction Individualize Twice RDA (30 mg) especially with significant diarrhea is present 2 times RDA

Sodium Potassium Calcium Phosphorus Fluid Iron Zinc Vitamins

AIDS and Dialysis 1.4-2.0 gm/kg actual or usual body weight 45-50 kcal/kg actual or usual body weight < 30% of kcal/modify type of fat based on fat malabsorption 2 to 4 gm/day 2-3 gm/day PD may need supplements 1-1.5 gm/day 10-12 mg/gm protein Urine output plus 1000-1200 cc Individualize Individualize Same as non-AIDS dialysis patient

Reference: Plourd D: Nutritional Management of the Dialysis Patient with AIDS. J Ren Nutr 5(4):182-193, 1995

3-8

HARRIS-BENEDICT FORMULA FOR DETERMINING BASAL ENERGY EXPENDITURE* Female (kcal) = 655 + (9.6 x Body Weightkg) + (1.8 x Heightcm) - (4.7 x Ageyrs) Male (kcal) = 66 + (13.7 x Body Weightkg) + (5.0 x Heightcm) - (6.8 x Ageyrs) * May overestimate calorie needs/reported to overestimate resting metabolic rate by 10-15%. Resting Energy Requirements During Acute Illness = BEE x Adjustment Factor Acute KD Energy Requirements = Estimated BEE x Adjustment for Illness x 1.25 SUGGESTED ADJUSTMENT FACTORS FOR ENERGY NEEDS DURING ACUTE ILLNESS* Bone Fractures Burns (% burned) 0-20%/21-40%/41-100% Elective Surgery - Day 1-4/Day 18-21 Fever Infection, Mild/Moderate/Severe Maintenance Hemodialysis Malnutrition (Chronic, severe) Multiple Organ Failure Nondialyzed CKD Peritonitis, Soft Tissue Trauma Postoperative (no complications) 1.2 - 1.25

1.2-1.25 1.0-1.5/1.5-1.85/1.85-2.05 1.0/0.95 x 7% for 1o F/ x 13% for 1o C > normal 1.0/1.2-1.4/1.4-1.6 1.0-1.05 0.70 1.2-1.4 1.0 1.15 1.0

* Even in hypermetabolic conditions, energy requirements rarely exceed 130% of BEE. Reference: Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins,1997 Page CP, et al: Nutritional Assessment and Support, 2nd Ed.Williams & Wilkins, 1994 3-9

ESTIMATED BODY WEIGHT AND ENERGY NEEDS IN PARA- AND QUADRIPLEGIA STEP 1 STEP 2 STEP 3

Determine SBW or ABW Modify weight for paralysis Paraplegia=subtract 5-10% from SBW/ABW Quadriplegia=subtract 10-15% from SBW/ABW To estimate energy expenditure in paraplegia or quadriplegia: Use reduced SBW/ABW in Harris-Benedict Formula

SBW = Standard body weight ABW = Adjusted body weight Note: Weight was changed from Hamwi IBW to SBW or ABW for consistency with the NKF K/DOQI guidelines. References: Peiffer SC, Blust P, Leyson JFJ: Nutritional Assessment of the Spinal Cord Injured Patient. J Am Dietetic Assoc 78:501, 1981

3-10

ESTIMATES OF CALORIES ABSORBED FROM PERITONEAL DIALYSATE The most accurate method of determining the caloric load from peritoneal dialysate is to measure the grams of glucose in the effluent and compare that to the grams of glucose that were infused. Several formulas have been published: Reference Grodstein, et al. KI, 19:564-567, 1981.

Formula Glucose absorbed = (11.3 x – 10.9) times L inflow times 3.4 where x = the average glucose concentration infused.

Bodner, et al. Adv in PD, 9:114-118, 1993

(1-D/Do) xi where D/Do is the fraction of glucose remaining and the xi is the initial glucose infused.

Example 4 L of 1.5% (1.36) + 4 L of 4.25% (3.8) solution = average 2.6% (11.3 x 2.6) – (10.9 x 8 liters) = 29.4 – 10.9 x 8L = 18.5 x 8L 18.5 x 8 L = 148 gms glucose 148 X 3.4 = 503 calories Infused = 4 L of 38 gm/L + 4 L of 13.6 gm/L=152 + 54.4 = 206 gm Measured remaining glucose = 1200 mg/dL in 10 liters effluent or 1200 x 10,000 mL/100,000 which = 1200 X 0.1 = 120 gm D/Do = 120/206 = 0.58 1–0.58 x 206 = 86.5gm x 3.4 = 294 kcal

Comment Developed before significant differences in membranes were recognized, but gives a rough glucose absorption/kcal estimate.

This considers dialysis modality and transport characteristics.

3-11

ESTIMATES OF CALORIES ABSORBED FROM PERITONEAL DIALYSATE (cont.) Reference Podel, et al. J Ren Nutr 10:93-7, 2000

Formula Example Comment With acute peritoneal dialysis in the critical care setting the mean total glucose absorbed was 43% ± 15%, suggesting that the Grodstein formula overestimates glucose absorption with 4.25% APD exchanges and underestimates glucose absorption with 1.5% APD exchanges.

Simple estimate

Glucose infused x 40% (CCPD) or 60% absorption (CAPD) 1.5% 1L=15 gm x 3.4 = 51 x 60%=31 kcal/L

4 L, 1.5% = 124 4 L, 4.25% = 346 Total kcal = 470

Rough estimate; doesn’t consider membrane transport characteristics or PD modality.

2.5% 1L=25 gm x 3.4 = 85 x 60%=51 kcal/L 4.25% 1L=42.5 gm x 3.4=144.5 x 60%=86.7 kcal/L

3-12

NATIONAL RENAL DIET FOOD CHOICE LISTS (CKD Not on Dialysis) (In development at press time) Food Group Choices High Protein +High P +High Na+ Vegetable- Low K+ Med K+ High K+ Breads/Starches + High Na+, P Fruit – Low K+ Med K+ High K+ Calorie Flavor Vegetarian Protein +High Na+ / K+ /P

Protein 6-8 6-8 6-8 2-3

Calories 50-100 50-100 50-100 10-100

Sodium 20-150 20-150 200-400 0-50

2-3 2-3 0-1

50-200 50-200 20-100

0-150 150-400 0-10

0-1 0 6-8 6-8

100-150 0-20 70-150 70-150

0-100 250-300 10-200 250-400

Potassium 50-150 50-150 50-150 20-150 150-250 250-550 10-100 10-100 20-150 150-250 250-550 0-100 0-100 60-150 250-500

Phosphorus 50-100 100-300 50-100 10-70

10-70 100-200 1-20

0-100 0-20 80-150 200-400

3-13

NATIONAL RENAL DIET FOOD CHOICE LISTS (CKD on Dialysis) (In development at press time) Food Group Choices High Protein +High Na, K+, P Dairy/Phosphorus Breads/Cereal/Grain +High Na+, P Fruit/Vegetables – Low K+ Med K+ High K+ Calories Flavor Vegetarian Protein +High Na+ /K+ /P

Protein 6-8 6-8 2-8 2-3 2-3 0-3

Calories 50-100 50-100 100-400 50-200 50-200 100-100

Sodium 20-150 200-500 30-300 0-150 200-400 1-50

0-1 0 6-8 6-8

100-150 0-20 70-150 70-150

0-100 250-300 10-200 250-400

Potassium 50-150 250-450 50-400 10-100 10-100 20-150 150-250 250-550 0-100 0-100 60-150 250-500

Phosphorus 50-100 100-300 100-120 10-70 100-200 0-70

0-100 0-20 80-150 200-400

3-14

VITAMINS FORMULATED FOR CKD PATIENTS Product

Vit C (mg)

B1 (mg)

B2 (mg)

Niacin (mg)

B6 (mg)

B12

Folic Acid

B5 (mg)

Biotin (mcg)

Dialyvite Dialyvite 800 Diatx* Nephrocaps Nephron-FA Nephrovite-Rx Nephrovite NephPlex-RxR TM RenaPlex

100 60 60 100 40 60 60 60 60

1.5 1.5 1.5 1.5 1.5 1.5 1.5 1.5 1.5

1.7 1.7 1.5 1.7 1.7 1.7 1.7 1.7 1.7

20 20 20 20 20 20 20 20 20

10 10 50 10 10 10 10 10 20

6 mcg 6 mcg 1 mg 6 mcg 6 mcg 6 mcg 6 mcg 6 mcg 6 mcg

1 mg 800 mcg 5 mg 1 mg 1 mg 1 mg 1 mg 1 mg 800 mcg

10 10 10 5 10 10 10 10 10

300 300 300 150 300 300 300 300 300

Fe (m g) -

Zinc (mg)

66 -

12.5 12.5

*(DiatxFe is also available and is comparable to Diatx plus 100 mg elemental iron.) References: Internet-Manufacturers’ Information

3-15

CONSIDERATIONS FOR A KOSHER DIET There are three basic concepts in Jewish dietary law: 1. The main concept governs the selection, preparation, and slaughtering of animal foods. a. Animals must chew a cud and have cloven hooves. Only the forequarters of these animals are acceptable. b. Eating of the blood (including arteries, veins, and muscle tissue) is forbidden. c. Turkey, chicken, goose, pheasant, and duck are kosher. Birds of prey are not kosher. d. Eggs from kosher birds are kosher, others are not. e. All kosher animals must be slaughtered in a specific way as described by the Torah. f. Fish with fins and scales are kosher; crustaceans, shellfish, and fish-like mammals are forbidden. 2. The second basic concept is the koshering of meat and poultry foods. a. Koshering removes all the blood through soaking and salting. Liver must be broiled. b. Koshering is done prior to cooking the food. 3. The third concept of the rules of kashrut is the separation of meat and dairy products. a. Meals either have a meat or a dairy focus. Fish is considered neutral and can be eaten with either. b. It is customary to wait 6 hours (Orthodox) after eating meat before ingesting dairy products. (1-5 hours for reformed conservative). c. Meat products can be eaten within a half hour to an hour after a dairy meal if the mouth is rinsed. d. Two sets of cookware, dishes, utensils, and drain boards are kept, one for dairy and one for meat. e. There are three categories of kosher food: meat, dairy, and pareve. Pareve are neutral foods that can be served with meat or dairy. Examples are fruits, vegetables, grains, beans, legumes, and their derivatives. Margarine is considered dairy unless marked “pareve.” Note: A Rabbi can be consulted for information about exceptions for medical conditions. Reference: Nichols D: What is a Kosher Renal Diet? J Ren Nutr 5(3):144-147, 1995

3-16

AVAILABLE FIBER, POTASSIUM, AND PHOSPHORUS IN COMMON HIGH FIBER CEREALS Cereal Cracklin’ Bran Bran Flakes, Post All Bran, Kellogg’s Extra Fiber Grape-Nuts Multi-Bran Chex, General Mills Quaker Oat Bran Shredded Wheat-n-Bran 100% Bran, Post Oat Bran, Cooked

Serving Size (cup) ¾ ¾ ½ ½ 1 1¼ 1¼ 1/3 1

Fiber (gm)

K+ (mg)

Phos

6.5 5.3 15.0 5.0 6.4 6.0 7.9 8.3 5.7

255 185 300 178 191 257 248 274 201

187 152 287 138 173 306 235 236 261

Reference: Internet: U.S. Department of Agriculture, Agricultural Research Service, 1999 Database for Standard Reference, Release 13. Nutrient Data Laboratory Home Page: http://www.nal.usda.gov/fnic/foodcomp

3-17

COMPOSITION OF MILK AND SUBSTITUTES (1 fluid oz serving unless indicated) Product Coffee Rich Coffee-Mate DariFree Beverage Mix (4 oz) Farm Rich Half & Half, 1 Tbsp. Light Cream, 1 Tbsp. Milk, 2% Milk, 1% Milk, Skim Milk, 3.25% Mocha Mix Mocha Mix Frozen Dessert Polyrich

kca l 44 40 181 36 20 29 15 12 11 19 38 148 44

CHO (gm) 4.4 4.0 42.2 2.2 0.6 0.5 1.5 1.5 1.5 1.5 2.4 17.9 4.4

PRO (gm) 0.0 0 0 0 0.4 0.4 1 1 1 1 0.2 0.6 0

FAT (gm) 3.2 2.0 0 3.0 1.7 2.9 0.5 0.3 0.05 1 3.2 7.6 2.6

Na+ (mg) 22 0 231 14 6 6 15 15 16 15 14 81 14

K+ (mg) 12 50 N/A 28 19 18 47 48 51 46 38 105 24

P (mg) 10 14 0.1 18 14 12 29 29 31 28 16 NA 10

Ca++ (mg) 0 0 150 0 16 14 37 37.5 38 36 2 NA 0

References: Internet: U.S. Department of Agriculture, Agricultural Research Service, 1999 Pennington JAT: Food Values of Portions Commonly Used, 17th Ed. Lippencott, 1998 Manufacturers’ Information

3-18

Chapter 4: SPECIAL CONSIDERATIONS FOR THE DIABETIC PATIENT

COMMON SYMPTOMS OF DIABETES Type I Type II Frequent urination* Drowsiness* Abnormal thirst* Itching Unusual hunger Blurred vision* Rapid weight loss Excess weight Irritability Tingling in feet* Obvious weakness Easily fatigued* Fatigue Skin infections* Nausea and vomiting Slow healing* 15-20% inherited Family history of DM

COMMON TREATMENTS OF DIABETES Type I Type II Insulin (often use Diet modification multiple shots) Exercise Diet modification Oral Agent/Insulin Exercise Blood sugar tracking Frequent BG tracking Education Education

*Common to both types DEFINITIONS OF DIABETES: Type I: Type I diabetes (formerly insulin dependent) is characterized by insulin deficiency that results from the destruction of beta cells of the pancreas, usually by an autoimmune process. Type II: Type II (formerly non-insulin dependent) is more common and is characterized by insulin resistance or decreased tissue glucose uptake in response to insulin. There is an insulin secretory defect that makes it impossible for them to release enough insulin to compensate for the insulin resistance. Gestational Diabetes Mellitus: This type of diabetes is one that is characterized by any glucose intolerance that first occurs or is recognized during pregnancy. Impaired Glucose Tolerance: Impaired glucose tolerance and impaired fasting glucose (IFG) are not considered as absolute diabetes but they are risk factors for later development of diabetes and cardiovascular disease. IFG is defined as a glucose concentration of >140 but <200 mg/dL 2 hours after ingestion of a 75 g glucose load or when fasting plasma glucose is >110 but <126 mg/dL. 4-2

STAGES OF DIABETIC NEPHROPATHY Stage 1: Hyperglycemia leads to increased kidney filtration due to osmotic load and toxic effects of high blood glucose. There is increased GFR with enlarged kidneys. Stage 2: Clinically silent phase, but continued kidney hyperfiltration and hypertrophy. Stage 3: Microalbuminemia (defined as 30-300 mg/day (20-200 mcg/min) loss of albumin in urine. With microalbuminemia 20% develop nephropathy within 5 years on standard care, 50% do not progress. Microproteinemia is a better predictor of progression in Type I than Type II. Microalbuminuria is a predictor of increased macrovascular disease. Microalbuminuria is associated with higher than recommended HbA1c levels (> 8.1%) Stage 4: Overt Nephropathy Almost always with hypertension, > 300 mg/day of albumin in the urine, about 10% have nephrotic range of proteinuria; GFR is decreased. Stage 5: CKD needing renal replacement therapy Over 30 years, >25% of patients with Type I DM progress to this stage. Over 25 years, about 8% of patients with Type II progress to this stage. Treatments to Slow Progression: ACE inhibitors (reduce microalbuminuria and the progression, independent of hypertension). Angiotensin II blockers may also be effective Mild protein restriction (0.6-0.75 gm/kg) (Some recommend up to 0.8 gm/kg) 4-3

RECOMMENDED DIETARY MODIFICATION IN DIABETIC NEPHROPATHY Stage of Disease Pre-clinical nephropathy Stage 1-2-3 Progressive nephropathy Stage 4

Hemodialysis

Peritoneal Dialysis

% Calories as CHO 50 - 60% Up to 40 gm fiber Achieve and maintain desirable body weight 55 - 65% Up to 40 gm fiber Achieve and maintain desirable body weight

% Calories as Fat ≤30% total calories as fat ≤10% saturated fat 6-8% polyunsaturated fat < 300 mg cholesterol/day ≤30% total calories as fat ≤10% saturated fat < 300 mg cholesterol/day

% Calories as Protein ~12 - 15% *

50 - 60% Low glycemic index ↑ fiber ~35 - 40% oral ~15% dialysate

≤30% total calories as fat ≤10% saturated fat

~12 - 20% *

≤30% total calories as fat

~12 - 20% *

~ 10% (50% HBV); replacement of urinary losses or 0.8 - 1.0 gm/kg if not replacing urinary losses)* Liberalize during periods of catabolic stress

*Liberalize protein allowance to 1.2 - 1.5 during catabolic stress. K/DOQI Recommendations for CKD not on dialysis: See page 3-5 Reference:

Mitch WE, Klahr S, Eds: Nutrition and the Kidney Little, Brown and Co., 1993 Kaysen G: Nutritional Management of Nephrotic Syndrome. J Ren Nutr 2:50, 1992 Stover J Ed: Clinical Guide to Nutrition Care in End-Stage Renal Disease, ADA 1994

4-4

TYPES AND ACTIONS OF INSULIN Type Crystalline zinc, unmodified, regular insulin Concentrated Regular Iletin II U 500 Insulin glargine

Onset 30-60 min

Peak 2-4 hours

Duration SC: 6-8 hours IV: 30-60 min

2 hours

6-8 hours

24 hours

Insulin lispro Insulin zinc suspension

15 min 1-2½ hr

30-90 min 7-15 hours

5 hours or less About 22 hours

Insulin zinc suspension extended (Ultralente)

4-8 hours

10-30 hours

>36 hours

Insulin zinc suspension, prompt (Semilente) Isophane insulin suspension (NPH)

1-1½ hours

5-10 hours

12-16 hours

1-1½ hours

4-12 hours

Up to 24 hours

Isophane insulin suspension/Injection

30-60 min

4-8 hours

24 hours

Names Pork Regular Insulin and Iletin II, Beef/Pork: Regular Iletin I Human: Humulin R, Novolin R, Velosulin For people who need more than 200 units of insulin per day; not for IV use Lantus - Given at bedtime provides better blood glucose control throughout the day Humalog (rDNA origin) Beef: Lente Insulin Pork: Lente Iletin II, Lente L Beef/Pork: Lentin Illetin I Human: Humulin L/Novolin L Ultralente Humulin U

Beef: Semilente Insulin Beef/Pork: Iletin I Semilente Beef: NPH Insulin; Pork: NPH-N, Pork NPH Iletin II Beef/Pork: NPH Iletin I Human: Humulin N, Novalin N Human: Humulin 50/50, Humulin 70/30, Novalin 70/30

NOTE: Time of onset/peak/duration may vary greatly among patients and is affected by dose/source/site of injection/exercise of the injection area (arm, leg)/insulin antibodies. Because the kidney is the site of insulin degradation, the onset, peak and duration may be altered in CKD. References: PDR Nurses Handbook, 3rd Edition, Medical Economics Company, 1998 4-5

ORAL HYPOGLYCEMIC AGENTS Type

Acarbose: Precose

Acetohexamide: Dymelor Chlorpropamide: Diabinese Glimepiride: Amaryl Glipizide: Glucotrol Glucotrol XL Glyburide: Diabeta, Micronase Glynase PresTab Metformin HCL: Glucophage Pioglintazone: Actos Repoglinide: Prandin Rosiglitazone: Avandia Tolazamide: Tolinase Tolbutamide: Orinase

Onset

Duration

2-hour half-life

1 hour 1 hour

12-24 hours 60-72 hours

1 hour 10-30 min

24 hours 24 hours

2-4 hours 1 hour Peak 1-3 hr

16-24 hours 12-24 hours 9-17 hours half-life 1½-5

2 hours 30 min 1 hr 4-6 hours 1 hour

24 hours 4 hours 24 hour 12-24 hours 6-12 hours

Other

Delays CHO digestion, does not incr insulin. Taken w/ meals, excreted in urine/stool. Treat low blood sugar carefully Excreted through kidneys Long duration; caution in aged/CKD; hyponatremia potential Taken 30 minutes before meals. Metabolized in liver; excreted in urine; low toxicity; caution in elderly Metabolized in liver; 50-200 X more potent than other agents; ↓ toxicity; caution in elderly Onset/duration not clearly defined; food delays onset/peak; given w/ meals; decr insulin resistance. Not for CKD Takes 3 months to reach steady state. Take 15-30 minutes before a meal, good for erratic meals Takes 3 months to reach steady state. Absorbed slowly, possibly fewer side effects Most benign; totally inactivated; useful in CKD

Reference: On the Cutting Edge: Diabetes Care and Education 10, November, 1989 (ADA)

Campbell: How Oral Agents are Used in Treatment of Type II Diabetes. Pharm Times 53:32-40, 1987 Skidmore-Roth L: 2000 Mosby’s Nursing Drug Reference, Mosby, 2000 Hodgson BB, Kizior RJ: Saunder’s Nursing Drug Handbook, 1999

4-6

GLYCATED HEMOGLOBIN (HbA1c) Glycation is the non-enzymatic addition of a sugar residue to the amino groups of protein, specifically the hemoglobin protein. The formation of glycated hemoglobin is irreversible and is unaffected by exercise and sudden shifts in blood glucose (BG) levels. Because the erythrocyte is freely permeable to glucose, the rate of glycation is proportional to the concentration of glucose. The life span of the average blood cell is 120 days and HbA1c is formed by the attachment of glucose to the N-terminal end of each β chain of the hemoglobin molecule. The amount of HbA1c, therefore, represents the integrated values of glucose over the previous 100-120 days. Obviously, any factor that reduces the life span of the erythrocytes, also reduces the glycated hemoglobin. The Diabetes Control and Complications Trial (DCCT) research group reports the following relationship between glycated hemoglobin (% A1c) and average blood glucose (BG) during the previous 2-3 months: a 1% change in HbA1c = a 30 mg/dL change in average BG. In the past, the clinical utility of glycated hemoglobin measurements in CKD was controversial. Early studies showed no correlation between glycated hemoglobin and other indicators of blood glucose control in uremic subjects. The lack of correlation is attributable, in part, to analytical interferences of altered hemoglobin found in uremic blood. Using ion-exchange chromatography, HbA1c values are often more directly correlated to urea and creatinine than to glucose. Measurement of HbA1c with the use of analytically specific methods can accurately reflect plasma glucose control in uremic patients as long as the HbA1c values are interpreted in view of the potentially shortened erythrocyte survival time. Reference:

Bruns DE, et al: Specific Affinity-Chromatography Measurement of Glycated Hemoglobin in Uremic Patients. Clinical Chemistry 30(4):569-571, 1984 Mosby’s Diagnostic and Laboratory Test Reference, 4th Ed, 1999

4-7

HYPOGLYCEMIA Causes: Excess circulating insulin, inadequate food intake, physical activity, drug interactions, glucose-free dialysate. Symptoms: Blood pressure may increase or decrease by 20-30 mmHg, pulse may fluctuate, sweating, cool/pale/moist skin, dizziness, fainting progressing to coma, slurred speech, tremor progressing to convulsion, headache, nervousness, restlessness, irritability, diminished mentation, weakness (similar symptoms are present in hypotensive episodes on dialysis except that systolic blood pressure drops below 100 mmHg). Hypoglycemic Protocol - Outpatient 1. If the blood glucose is <70 mg/dL, give 15 grams of CHO: ½ cup of regular soda ½ cup apple juice 5 lifesavers 3 sugar cubes or 3 packets of sugar 3 glucose tablets 1 tube Glutose 15 2. Recheck blood glucose in 15 minutes, if <70 mg/dL, repeat steps above. 3. Follow-up with a more substantial snack or meal containing CHO, pro, fat, especially if the next meal is more than 2 hours away.

NOTE: Patients on Precose and oral sulfonylureas or insulin must be treated with glucose. Precose inhibits the breakdown of sugar (sucrose) to glucose and slows the absorption of sucrose or fructose (found in sodas or fruit juices) making them less effective in treating hypoglycemia.

References:

Moore MC: Nutritional Care. Mosby’s Pocket Guide Series, 4th Ed, 2001 Robels F: On the Cutting Edge: Diabetes and Care and Education, ADA, 10:2, 1989

4-8

MODIFICATIONS FOR ACUTE ILLNESS IN INSULIN DEPENDENT DM General Goals Suggested 15 gram CHO Sick Day Foods 1. Check blood glucose frequently, q 2-4 hrs ½ cup regular gelatin 2. Ingest 10-15 gm CHO every 1 to 2 hours. ½ cup sherbet or sorbet 3. If symptoms of diarrhea, vomiting, or fever, 1 Frozen juice bar take small amounts of fluids every 15-30 min 6 unsalted top crackers 4. Contact the MD if unable to ingest and retain 4 pieces of melba toast CHO-containing foods and fluids for more than 1 cup reduced-salt chicken noodle/rice/pasta soup 4 hours, if BG is fluctuating widely, or illness ¼ cup regular pudding or custard lasts more than 24-48 hrs. ¾ cup ginger ale ½ cup regular lemon-lime soda ½ cup apple juice ⅓ cup cranberry juice cocktail or grape juice 5 lifesavers References: Moore MC: Nutritional Care. Mosby’s Pocket Guide Series, 4th Ed, 2001 Hands, ES: Nutrients in Foods. Lippencott Williams & Wilkins, 2000

4-9

FOOD GLUCOSE EQUIVALENT TO 15 GM CARBOHYDRATE Source Gelatin, Reg Honey Orange Juice Gatorade BD Tablets Dextrosol Glutose

Amount ½ cup 1 Tbsp. ½ cup 1 cup 3 Tabs 5 Tabs 40 gm

Glucose (gm) 6 7.1 6.6 5.8 15* 14* 16*

CHO (gm) 17 17.3 12.8 15.2 15 14 16

KCAL 71 64 54 60 60 56 64

Fluid ½ cup ½ cup 1 cup -

Potassium (mg) 30-110 230-250 37

* Preferred choices, all available as glucose. DO NOT USE fruit or soft drinks that contain only high fructose corn syrup to treat hypoglycemia. The major carbohydrate source should be glucose, dextrose, or sugar. Reference: McKinley H: On the Cutting Edge: Diabetes Care and Education, ADA, 14(4):23, 1992

Acceptable food equivalents for renal patients include: 2 tsp sugar or jelly, 6-8 jelly beans or lifesavers (chewed), ½ cup apple, grape juice, or cranberry juice. Reference: Levine S: On the Cutting Edge: Diabetes Care and Education, ADA, Winter, 1985

4-10

DIABETIC GASTROPARESIS Diabetic gastroparesis and delayed gastric emptying are linked to unpredictable nutrient absorption and poor food intake causing wide fluctuations in blood sugar by compromising the effects of oral agents and exogenous insulin. Small, frequent feedings, medications, and interventions as listed below, may ease the symptoms of gastroparesis. Gastroparesis is characterized by vomiting of undigested food several hours after ingestion. Common symptoms include vague abdominal distress, heartburn, nausea, vomiting, early satiety, abnormal food digestion and absorption, increased fluctuations in blood sugar. Intervention Frequent, small meals Metoclopromide HCL Loperamide HCL Cisapride: Propulsid Jejunostomy Tube Erythromycin Domperidone Motilin antagonist References:

Effect Helps minimize symptoms. Low fat may help. Advise pt to chew foods well Stimulates motility of upper GI tract w/out increasing gastric, bilary or pancreatic secretions. May help diarrhea. High incidence of CNS side effects Increases gastric contractions, relaxes pyloric sphincter, anti-emetic actions Reduces gastric retention in some diabetic patients. (Not recommended in CKD due to potentially fatal dysrhythmias) Overcomes gastric stasis, can provide symptomatic relief Systemic treatment of gastropariesis Prokinetic GI motility drug, blocks dopaminergic receptors in upper alimentary tract, stimulating the motility of the esophagus, stomach, & upper small intestine Same as Domperidone

Daugirdas JT, Ing TS: Handbook of Dialysis, 2nd Edition, Little, Brown, & Co., 1994 Beaven K. Gastroparesis and Jejunal Feeding. J Ren Nutr 9(4):202-205, 1999 Skidmore-Roth L: 2000 Mosby’s Nursing Drug Reference, Mosby, 2000

4-11

OTHER NUTRITION ISSUES FOR DIABETICS Standard calorie-specific meal patterns have traditionally been used for diabetic patients. The current American Diabetes Association (ADA) recommendations suggest that “consistent carbohydrate meal plans” may be the most appropriate method for maintaining metabolic control. These meal plans are based on a consistent carbohydrate (CHO) content for each meal rather than specific calorie levels for each meal. The CHO content for each specific meal would be consistent from day to day (breakfast = breakfast, lunch = lunch, dinner = dinner, snack = snack) although the CHO content could differ between breakfast, lunch, and dinner. It is also suggested that the use of “ADA diet” terminology be discontinued since the ADA no longer endorses a single meal plan or absolute percentages of macro nutrients. Further, meal plans such as “no added sugar,” “low sugar” and “no concentrated sweets” are no longer appropriate. These general meal plans do not reflect current diabetes nutrition therapy. They unnecessarily restrict sucrose and may falsely imply that simple restriction of sucrose sweetened foods will improve blood sugar control. Clear or Full Liquid Diet – Initiate 200 gm CHO per day in equally divided amounts at meal and snack times using regular, sweetened liquids and adjust diabetic medications as needed. Post-Surgery - Initiate oral intake quickly, as tolerated, with rapid progression to solid foods. Catabolic Illness - Continuous, careful monitoring of nutritional and glycemic status is critical in addition to providing adequate nutrition without exacerbating hyperglycemia or overfeeding the patient. Reference: Schafer, R.G. et al. Translation of the diabetes nutrition recommendations for health care institutions: Position Statement. JADA 97(1):43-53, 1997

4-12

Chapter 5: SPECIAL CONSIDERATIONS FOR THE ELDERLY PATIENT

EDUCATION CONSIDERATIONS FOR THE ELDERLY 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Be considerate. Start by asking the patient to tell you if they get tired or overwhelmed. Include family members or caretakers in the diet instruction as permitted by the patient. Speak directly to the patient in a strong, clear voice. Keep the instructions simple and short. Then, ask questions to ascertain the patient’s understanding before moving on. Limit the time you spend each session and present only 2-3 points at each session. Review the previous session briefly before moving on to the next area of instruction. Use large print materials, pictures, and food models to illustrate your points. Give written materials to back up verbal information. If changing medications such as binders, calcium, or vitamins, provide written follow-up to a verbal instruction. Because of a tendency to decrease intake (both in CKD and aging) it is critical to be as liberal as possible with the meal plan. Recognize that you will probably not change a lifetime of eating patterns and include the foods the patient has always eaten. Recognize the decrease in taste/smell, and allow the patient as much flavor enhancement as possible.

5-2

D-E-T-E-R-M-I-N-E: A NUTRITION CHECKLIST FOR THE ELDERLY D

Disease - physical or emotional issues that change the way the patient eats.

E

Eating poorly - too little or too much can cause nutrition problems.

T

Tooth loss/mouth pain - are teeth and gums healthy, do dentures fit?

E

Economic hardship - many elderly persons have poverty level incomes.

R

Reduced social contact – 1/3 live alone; social contact influences morale/intake.

M

Multiple medicines - means greater chance for nutritional side effects.

I

Involuntary weight loss or gain - an important warning sign.

N

Needs assistance in self-care - 1 in 5 needs help (shopping/cooking/walking).

E

Elder years above 80 - as age increases, generally so do the problems.

This acronym was developed by The Nutrition Screening Initiative. (Nutrition Interventions Manual for Professionals Caring for Older Americans, Washington, D.C.; Nutrition Screening Initiative, 1992) The original was written for patient self assessments, but was adapted to provide a checklist of risk factors for interviewing elderly patients. Leung and Dwyer adapted this tool for CKD patients. Reference: Simko M et al: Nutrition Assessment: A Comprehensive Guide for Planning Intervention, ASPEN Publications, 1995 Leung J, Dwyer J: Renal DETERMINE Nutrition Screening Tools for the Identification and Treatment of Malnutrition, J Ren Nutr 8(2): 95-103, 1998 5-3

POTENTIAL INFLUENCES ON NUTRITION STATUS IN THE ELDERLY Physical Dental problems Swallowing disorders Excretion problems Decreased activity Physical weakness/limits Loss of sensations Lactose intolerance Drug interference Abnormal digestion Chronic disease Thyroid dysfunction Nutrient deficiencies Alcohol consumption

Psychological Depression Anorexia Personal taste preferences Lifetime eating patterns Lack of socialization Dementia Loss of spouse

Social Financial constraints Inconvenient food preparation Difficult adaptation to change Erroneous dietary beliefs Susceptibility to fad claims

References: Chernoff R: Meeting the Nutritional Needs of the Elderly in the Institutional Setting. Nutrition Reviews 52(4): 132, 1994 Grodner M, Anderson S, DeYoung S: Foundations And Clinical Applications of Nutrition: A Nursing Approach Mosby, 2000

5-4

PHYSIOLOGICAL CHANGES IN THE ELDERLY Area Mouth

Change Mouth pain, ill-fitting dentures

Result Pt uses soft/liquid foods with limited nutrients

Sensory

Loss of taste and smell, especially sweet and salty

Loss of papillae/taste buds on tongue, difficulty with ↓ salt diet, foods taste bitter

Digestive Tract

Decreased esophageal motility Decreased peristalsis Bowel muscle atrophy Decreased thirst sensation

Dysphasia, pain, and regurgitation Slow movement through GI tract, sense of fullness, constipation Coupled with inactivity, causes constipation Dehydration

Organs

Decreased hepatic function Decreased kidney function

Decreased protein synthesis Can advance to CKD with a health crisis

Muscle

Decreased skeletal muscle mass

Difficult ambulation, inactivity can lead to negative nitrogen balance, decreased ability/strength to prepare meals

Skeleton

Osteoporosis, bone mineral loss

Easy fractures compounded by further muscle loss from inactivity

Decreased alertness, confusion

Difficulty with activities of daily living; target for fad foods/OTC medications

Mental

Reference: Simko M, et al:. Nutrition Assessment: A Comprehensive Guide for Planning and Intervention, ASPEN Publications, 1995 5-5

BODY COMPOSITION CHANGES IN THE ELDERLY Age 25 yrs 70 yrs

% Fat 20% 36%

% Cell Mass 47% 36%

% Bone Mineral 6% 4%

Other 27% 24%

Reference: Gregerman RI, Bierman EI: Textbook of Endocrinology, RH Williams, Ed. WB Saunders Co., 1974

DECREASE IN PHYSIOLOGICAL FUNCTION AT 80 YEARS OF AGE Physiological Function Nerve Conduction Velocity Basal Metabolic Rate Standard Cell Water Content Cardiac Index Standard GFR Standard Renal Plasma Flow

% Decrease From Age 30 15 - 20% 20% 20% 30% 45% 53%

This information is included to help differentiate normal changes of aging from those changes that could indicate disease or malnutrition. Reference:

Tobin JD: Normal Aging - The Inevitable Syndrome, The Quality of Life, The Later Years, Brown LE, Ed. Publishing Sciences Group, Inc. 1975

5-6

INCIDENCE OF MALNUTRITION IN THE ELDERLY Reference Mowe, et al. 1994

Population 311 elderly, hospital admission

Parameters Albumin, body mass index, MAMC, TSF, intake record

Abbasi, et al. 1993

2,811 skilled nursing facility (SNF) -VA

Albumin, weight

Mowe, et al. 1991 Thomas, et al. 1991

121 elderly, acute care facility 61 elderly, ECF/ rehab hospital

Pinchofsky, et al. 1987

227 elderly, ECF

Albumin, weight, MAC, MAMC, TSF Albumin, wt, TSF, MAC, MAMC, Hgb, TLC, nutrition index Albumin, wt, TSF, MAC, MAMC, prealbumin, retinol binding protein, TLC, Hct/Hgb

Incidence 52.9% undernourished (M) 60.6% undernourished (F) Low intake-65% (M) 69% (F) 11.8% underweight 27.5% hypoalbuminemic 54.5% undernourished 54% malnourished on admission, 37% still malnourished at 2 months 52% PE malnutrition 24% adult kwashiorkor 19% mixed 9% marasmus

Reference: Simko M, et al: Nutrition Assessment - A Comprehensive Guide for Planning Intervention. Aspen Publishers, 1995

5-7

SUBJECTIVE GLOBAL ASSESSMENT (SGA information can be found on page 1-34 to 1-41) Editorial Note: It is critical to assess tissue (fat and muscle) loss objectively in the aged. The tissue loss seen in the aging patient mimics the tissue loss seen in malnutrition. In view of this, some of the other parameters of SGA may become more important in elderly patients. Pay special attention to weight changes, gastrointestinal symptoms, alterations in food intake, and a comparison of actual nutrient intake to recommended levels. Question the patient carefully to get his/her views on the significance of changes and their duration. Some research indicates that SGA can overestimate malnutrition in as many as 20% of elderly patients. Reference: Ek AC, et al: Interrater variability and validity in subjective nutritional assessment of elderly patients. Scand J Caring Sci 10(3):163-168, 1996

5-8

Chapter 6: HYPERLIPIDEMIA IN CHRONIC KIDNEY DISEASE

GENERAL PATTERNS OF HYPERLIPIDEMIA IN CKD Pattern

Distribution of lipid/apolipoproteins in CKD: CKD/HD: mild to moderate hypertriglyceridemia, low to mildly elevated cholesterol/LDL, low HDL PD: triglycerides (TG) may be very elevated, HDL often normal, cholesterol WNL to high Transplant: High LDL/cholesterol especially with cyclosporin, HDL often normal, TG may be very high Nephrotic syndrome: low to normal HDL, high cholesterol/LDL, high triglyceride levels are common.

Mechanism

Mechanisms probably include both increased hepatic production and impaired removal of circulating triglyceride-rich lipoproteins (VLDL, LDL). Altered carbohydrate metabolism with concurrent hyperinsulinemia, and peripheral insulin resistance may also contribute.

Treatment (See pages 6-4 to 6-5)

Moderate diet modification as outlined for the general population. Weight control and reduced intake of carbohydrate can minimize the overproduction of LDL/triglycerides. Exercise, as tolerated, may help. Diet modifications for maintaining acceptable nutrition status takes priority over diet for hyperlipidemia. It may be difficult to limit fat to < 30% of total calories when protein levels are dictated and calorie needs are high. Nephrotic Syndrome: low fat, high complex carbohydrate, salt restricted with other nutrients as described in Chapter 3. Long term use of pharmacologic lipid lowering agents requires careful consideration/monitoring in CKD.

References: Mitch WE, Klahr S, Eds: Nutrition and the Kidney, Little, Brown & Co., 1993 Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997

6-2

PATIENTS AT RISK FOR DEVELOPING CARDIOVASCULAR COMPLICATIONS High serum lipids and LDL cholesterol have been shown to be important risk factors for coronary heart disease. Extrapolation of general risks and guidelines to the CKD population are not clear; however, the lipid disorders of CKD may contribute to the high incidence of atherosclerosis and CV disease in this patient population. A conservative treatment approach for dyslipidemia in CKD patients results from the lack of evidence that aggressive treatment makes a significant difference. Further studies are being undertaken to establish appropriate treatment parameters. In addition ,research is under way to elucidate the role of homocysteine in aggravating cardiovascular complications. 1.

Patients with established coronary artery disease

2.

Patients with diabetes mellitus

3.

Patients with LDL cholesterol > 60 mg/dL (100-160 mg/dL depending on risk factors-see pg.6-5)

4.

Patients with markedly elevated triglycerides (>500 -1000 mg/dL)

5.

Young/middle-aged male patients w/significant hyperlipidemia/prospect of long term dialysis

6.

Patients with nephrotic syndrome. Every effort should be made to decrease proteinuria since hyperlipidemia correlates with proteinuria and is inversely related to serum albumin. Pharmacologic therapy is almost always necessary. A soy-based vegetarian type diet with fish oil has been shown to decrease total cholesterol, LDL cholesterol, and triglycerides

Reference: Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997

6-3

NATIONAL CHOLESTEROL EDUCATION PROGRAM (NCEP), 2001 Focus on Multiple Risk Factors

Modifications of Lipid/Lipoprotein Classification Support for implementation

LDL Goals depend on risk factors

Raises persons with DM without CHD to risk level of CHD risk equivalent Uses Framingham projections of 10 years CHD risk to identify those who need more intensive treatment Identifies pts w/multiple risk factors (metabolic syndrome) for intense Theraputic Lifestyles Changes (TLC) Intensity of risk reduction therapy adjusted to person’s absolute risk Identifies LDL cholesterol as primary target of therapy Identifies HDL <40 mg/dL as the at risk level (up from <35 mg/dL) Lowers TG classification cutpoints to focus on moderate elevations Recommends complete lipoprotein profile (LDL, HDL, TG) as initial test Encourages use of plant sterols and viscous fiber as diet options for lowering LDL Provides strategies for promoting adherence to TLC and drug therapy Recommends treatment beyond LDL lowering for TG ≥200 mg/dL CHD and CHD Equivalents (DM) <100 mg/dL Multiple (2+) risk factors <130 mg/dL Zero to one risk factor <160 mg/dL Major Risk Factors that Modify LDL Goals: Cigarette smoking, hypertension, HDL <40 mg/dL, Family history of CHD (men-1st degree relative <55 years; women -1st degree relative <65 years), age (Men >45; women >55); DM; life habit risk factors (obesity, physical inactivity, atherogenic diet); emerging risk factors (lipoprotein -1, homocysteine, prothrombiotic and proinflammatory factors)

6-4

TARGET LIPID LEVELS Cholesterol Total LDL HDL

Optimal < 200 mg/dL < 100 mg/dL > 60 mg/dL

Borderline 200-239 mg/dL 130-159 mg/dL

High > 240 mg/dL 160-189 mg/dL

Very High >190 mg/dL

Fasting levels for adults, >20 years. Panel should be obtained q 5 years. If non-fasting, only total/HDL will be usable.

THERAPEUTIC LIFESTYLE CHANGES (TLC) Diet TLC

Total Fat* 25-30%

Sat. Fat* <7%

Polyunsat. Fat* up to 10%

Monounsat. Fat* up to 20%

CHO

Protein

50-60%

15%

CHOL (mg/day) <200

Fiber (g/day) 20-30

Total Kcal To maintain desirable BW

* Percentage of total calories. TLC: enhancing LDL lowering actions (use of plant stanols/sterols), increased soluble fiber (10-25 gm/day), weight reduction as appropriate, and increased physical activity. After 12 wks, if LDL goal not met, consider drug therapy. Major Risk Factors that Modify LDL Goals: Cigarette smoking, hypertension, low LDL, family history of CHD (men-1st degree relative <55 years; women-1st degree relative <65 years), age (Men > 45; women > 55), DM Reference: Adult Treatment Panel III - National Cholesterol Education Program (NCEP), NIH, National Heart, Lung, and Blood Institute, NIH Publication #01-3670, May 2001 6-5

ANTIHYPERLIPIDEMIC DRUGS Drug Bile Acid Sequestrants Cholestyramine Resins Questran Cholestipol Cholestid Colesevelam

Action Works in bowel, does not enter blood stream. Removes bile acids from biliary system, uses cholesterol to make bile acids. ↓ LDL by ~15-30% 0−↑ TG, ↑ HDL 3-5%

Adverse Effects* Gastrointestinal distress, constipation, decreased absorption of nutrients and other drugs. Do not use if TG are >400.

Dietary Needs Balanced diet , ↑ fiber, ↓ fat/cholesterol.

Fibric Acids Clofibrate-Αtromid-S Gemfibrozil-Lopid Fenofibrate-Lipidil

Interferes with hepatic synthesis of cholesterol/TG, ↑ rate of removal. ↓ TG by ~ 20-50%, ↓ LDL by ~ 5-20% ↑ HDL by 10-20%. Avoid in CKD - risk for myopathy/rhabdomyolysis

Most common: dyspepsia, gallstones, myopathy.

↓ fat/cholesterol, maintenance of desirable body weight; Taken with food/milk eases GI effects.

Do not use in severe kidney or liver disease.

* Incomplete list, most common and/or are nutrition-related side effects.

6-6

Drug HMG-CoA Reductase Inhibitors (Statins) Atorvastatin-Lipitor Cerivastatin-Baycol Lovastatin-Mevacor Fluvastatin-Lescol Pravastatin-Pravachol Simvastatin-Zocor

Action Inhibits early rate-limiting step in cholesterol synthesis. Levels decrease within 1-2 weeks, reaches lowest in 4-6 weeks.

Nicotinic Acid Nicolar, Nicobid Niacor, NiaBid Nico400, Nicotinex SloNiacin, Niaspan

Not well understood. Estimated to ↓ LDL by ~ 5-25%, ↓ TG 20-50% ↑ HDL by ~15-35%. Individual response depends on severity and etiology of lipidemia.

↓ LDL by ~18-55%, ↓ TG by ~ 7-30%, ↑HDL by ~ 5-15%

Adverse Effects* Myopathy, ↑ liver enzymes. Do not use in active or chronic liver disease. Do not use with cyclosporin, macrolide antibiotics, antifungal agents, cytochome P-450 inhibitors. Use caution with niacin and fibrates.

Dietary Need ↓ fat/cholesterol, weight control

Flushing, hyperglycemia/ glucose intolerance, upper GI distress, hyperuricemia/gout, activates peptic ulcers, hepatotoxicity. Do not use in chronic liver disease or severe gout. Caution: DM, peptic ulcer, hyperuricemia.

Adjust CHO intake, ↓ purines, limit alcohol, give with meals, liberal bland diet with antacid

* Incomplete list, most common and/or are nutrition-related side effects. References: Nursing Drug Handbook, Springhouse Corp, Pennsylvania, 1997 Physicians Desk Reference, Medical Economics Company, New Jersey, 1994 Simon & Schuster Interactive, The Pill Book on CD ROM, 1996 Adult Treatment Panel III - National Cholesterol Education Program (NCEP), NIH, National Heart, Lung, and Blood Institute, NIH Publication #01-3670, May 2001 6-7

APPROXIMATE CHOLESTEROL CONTENT OF COMMON FOODS* Food Source Bacon, 1 strip Beef, lean, 1 oz Bologna, beef, 1 slice Butter, 1 tsp. Chicken, white, 1 oz Dark, 1 oz Cheese, Cheddar, 1 oz Cottage Cheese, 4 oz Egg, 1 large Frankfurter, beef (8/lb) Halibut, 1 oz Ice Cream, 10% fat, ½ cup Lamb, lean, 1 oz Liver, beef, 1 oz Margarine, 1 tsp.

CHOL (mg) 5 25 13 11 24 26 30 17 272 35 12 30 20 111 0

Food Source Mayonnaise, 1 Tbsp. Milk, whole, 1 cup 2% 1% Skim Buttermilk, cultured Pork, 1 oz Peanuts, ½ oz Shellfish: Shrimp, 1 oz Crab, Lobster, 1 oz Soybean Oil, 1 tsp. Tuna, light, in water, 1 oz Turkey, white, 1 oz Dark, 1 oz Veal, 1 oz

CHOL (mg) 7 33 18 10 4 9 28 0 43 20 0 10 12 24 25

* Does not address levels of saturated fat. Values are calculated from data in reference. Reference: Pennington JAT: Food Values of Portions Commonly Used, Harper & Row, New York, 1998

6-8

Chapter 7: ANEMIA IN CHRONIC KIDNEY DISEASE

ANEMIA Anemia is described by the relationships between the number, size, and hemoglobin content of red blood cells (RBC). Normochromic, normocytic anemia is present in most patients with chronic kidney disease. TERMINOLOGY USED TO DESCRIBE CELL ALTERATIONS IN ANEMIA Term

Cell Characteristics

Normochromic

Normal hemoglobin content per cell

Hypochromic

Decreased hemoglobin content per cell

Hyperchromic

Increased hemoglobin content per cell

Normocytic

Normal cell size

Microcytic

Smaller than normal cell size

Macrocytic

Larger than normal cell size

Reference: Ravel R: Clinical Laboratory Medicine: Clinical Application of Laboratory Data, 4th Edition. Year Book Medical Publishers, Inc. Chicago-London, 1984

7-2

TYPES AND CHARACTERISTICS OF ANEMIA Anemia Classification Hypochromic Microcytic

Characteristics Iron deficiency anemia, most common anemia in CKD especially with EPO therapy

Normochromic normocytic Megaloblastic

Usually due to acute loss of red blood cells from hemorrhage or hemolysis. Anemia of chronic disease Folic acid/B12 deficiency usually due to long term inadequate dietary intake or deficient absorption/utilization. Responds to replacement of nutrients. Blood cells are larger than normal. Protein deficiency anemia is rare even in cachexia. Copper/heavy metal deficiency anemia is rare. Anemia is common in patients with low serum albumin for a variety of reasons.

Other

Reference:

Ravel R: Clinical Laboratory Medicine: Clinical Application of Laboratory Data, 4th Edition Year Book Medical Publishers, Inc. Chicago-London, 1984

7-3

LABORATORY VALUES USED TO DIAGNOSE ANEMIA Initiate Evaluation (K/DOQI) Hgb <11 g/dL, Hct <33% premenopause (F) or prepubertal (M); Hgb <12 g/dL, Hct <37% adult (M) or postmenopausal (F) Value Hematocrit (Hct)

Hemoglobin (Hgb)

Mean Corpuscular Volume (MCV) Mean Corpuscular Hemoglobin Concentration (MCHC) Mean Corpuscular Hemoglobin (MCH) Reticulocyte Count Reticulocyte Index

Iron Monitoring Parameters

Definition Volume of packed cells/100 mL blood (40% means 40 mL of red blood cells (RBC)/100 mL blood). K/DOQI Targets with EPO therapy: 33-36% Oxygen carrying protein of RBCs gm/100 mL (15.5 means 15.5 g Hgb/100 mL blood) K/DOQI Targets for EPO therapy: Hgb 11-12 g/dL Describes red cells in terms of volume per cell. Normal is 81-100 µm3* Measures concentration of hemoglobin in 100 mL of RBCs. Normal is 32-35% The hemoglobin content of each red blood cell. Normal is 27-31 pg/cell* Most sensitive indicator of red cell production/bone marrow activity; responds before hematocrit. Reported as a % of the total RBCs. Normal is 0.5 - 2% Indicates erythropoetic response in anemic or low Hct patients calculated as RI = Reticulocyte count (IU%) x patient Hct. normal Hct.If the RI is < 1.0 even with high reticulocyte count, marrow response is inadequate. Serum iron, serum ferritin, TIBC, % transferrin saturation (K/DOQI)

Test stool for occult blood Test for Occult Blood * Normal values are laboratory specific. The above values are general ranges. Reference: Treseler KM: Clinical Laboratory and Diagnostic Tests, 3rd Edition, Appleton Lange, 1995 NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1, Jan, 2001 7-4

INTERPRETATION OF IRON STATUS PARAMETERS Parameter Serum Iron Transferrin Saturation TIBC Ferritin (1 ng/mL = 8-10 mg stored iron)

Iron Deficiency Decreased Decreased Increased Decreased

Inflammation* Decreased Decreased Decreased Increased

Combination Decreased Decreased Normal Normal to increased

*Suspect inflammation when serum iron is decreased, transferrin saturation is decreased, and serum ferritin is increased. Ferritin is an acute phase reactant; therefore, synthesis is increased, independent of iron stores, in chronic or acute inflammation, fever, or liver disease. References: Foxen L: Monitoring for Infection and Inflammation During EPO Therapy. Presentation, 1993 Stivelman J: Optimization of Iron Therapy in HD Pts Treated with rHuEPO. Sem Dial 7:288,1994

7-5

IRON BALANCE IN CKD PATIENTS (K/DOQI) 1. Deficiency of erythropoietin in CKD causes anemia which is further aggravated by iron deficiency.

EPO therapy increases the rate of erythropoiesis and the demand for iron. 2. Maintain transferrin saturation (TS) ≥20% and serum ferritin ≥100 ng/mL during EPO therapy. Better response or equal response with lower doses may be achieved with higher iron stores (up to 50% TS or 800 ng/mL serum ferritin). 3. Measurement of iron parameters: Individual IV iron dose ≥1000 mg-wait 2 weeks after last iron administration; iron dose < 100-125 mg/week-no interruption of therapy needed; IV iron doses of 200-500 mg-wait at least 7 days. 4. Iron absorption is thought to be normal in CKD patients, but losses of up to 6 mg/day from blood testing, dialyzer/tubing waste, GI bleeding, and leakage of vascular access, exceed the amount of iron that can be absorbed from oral sources. In addition, inconvenient dosing and side effect may limit the use of oral iron. 5. CKD-prior to initiation of dialysis and PD, patients have minimal iron losses and many may be able to maintain iron stores by taking oral iron (≥ 200 mg elemental iron per day, divided into 2-3 doses in adults and 2-3 mg/kg/day in the pediatric patient). Absorption is inversely related to body iron stores and may decrease when ferritin >200 ng/mL and TS >20%. 6. Ionic iron salts (ferrous fumarate, sulfate, or gluconate) are inexpensive and provide known amounts of elemental iron. Other iron supplements have not been shown to be more effective or to have fewer side effects and they are generally more costly. K/DOQI opinion: Oral iron is not indicated when using IV iron. 7. Oral iron supplements should be ingested away from other medications and ≥2 hours before or ≥1 hour after meals. Vitamin C, in doses safe for CKD patients, does not enhance ferrous iron absorption. 8. Enhance compliance and avoid side effects of oral iron by using smaller, more frequent doses, increasing the dose slowly, changing the compound/product, or prescribing iron at bedtime. 9. A trial of oral iron is acceptable in HD, but most HD patients will require IV iron to maintain iron stores and Hgb/Hct especially on EPO. (See page 7-8) Reference: NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1, Jan, 2001 7-6

LABORATORY VALUES USED TO DIAGNOSE IRON DEFICIENCY IN CKD (K/DOQI) Total iron binding capacity, transferrin saturation (TS) and serum ferritin are the best indicators of iron stores and available iron for erythropoiesis, but do not absolutely define iron deficiency or iron overload.

Lab Test Serum Ferritin

Transferrin Saturation

Indication Reflects iron stored in liver, spleen, bone marrow reticuloendothelial cells Reflects iron that is readily available for erythropoiesis

Normal 12-300 µg/L

Indication of Iron Deficiency* <100 µg/L

35±10%

<20%

*In chronic kidney disease it has been suggested that iron stores must be sufficient (as above) to maintain a hemoglobin of 11-12 g/dL and a hematocrit of 33-36%. Some patients are able to sustain erythropoiesis and an acceptable hematocrit in spite of ferritin and TS levels less than above. In contrast, some patients are functionally iron deficient (respond to higher doses of iron) with laboratory levels greater than those above. Both serum ferritin and TS are most accurate in predicting iron deficiency or iron overload when they are extremely high or low. They are not perfectly sensitive or specific. The levels above are suggested guidelines for identifying CKD patients who may be iron deficient. Other laboratory tests that have traditionally been used to diagnose iron deficiency do not seem to increase the diagnostic specificity or sensitivity over the two parameters recommended above. Administration of IV iron can falsely alter serum ferritin and TS levels for 1-3 weeks post administration depending on the dose administered. The levels of ferritin or TS that indicate iron overload are not well defined but there does not seem to be any benefit (increased response to EPO or ability to use lower doses of EPO) in maintaining ferritin at >800 ng/mL or TS at >50%. Reference: NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1, Jan, 2001 7-7

ESTIMATION OF IRON NEEDS: Recommendations for Repletion 1. To increase the hematocrit from 25% to 35%, the amount of supplemental iron needed in the first 3 months of EPO therapy is approximately 1000 mg. Storage iron in the body is 800-1200 mg and 400 mg of iron are needed just to replace losses. The other 600 mg are needed to support the production of red blood cells to achieve the target Hgb/Hct. 2. After reaching target Hgb/Hct, 400-500 mg every 3 months is needed to maintain stores. 3. Oral iron alone is usually insufficient to meet these needs. 100-125 mg of IV iron at each HD treatment for 10-8 weeks is recommended to correct functional iron deficiency. A second course should be given if iron parameters remain low. The administration schedules of IV iron therapy range from three times per week to once every two weeks with the goal of giving 250-1000 mg of iron within a 8-12 week period. 4. Obtaining accurate measurement of TS and ferritin depends on the dose of IV iron: IV iron dose of <100-125 mg/week - no interruption of therapy is needed. Individual IV iron dose of ≥ 1 gram - wait at least 14 days after the last IV iron administration. IV iron dose of 200-500 mg - wait at least 7 days after the last IV iron administration. 5. Prevention of functional or absolute iron deficiency with maintenance doses of IV iron improves erythropoiesis. Maintenance doses of IV iron range from 25-100 mg/week for HD. 6. Iron supplementation should be temporarily withheld (up to 3 months) if iron stores are high (no known benefit from increasing TS >50% and/or ferritin >800 ng/mL). Once TS and ferritin drop back into target range, maintenance IV iron should be restarted at a dose reduced by 1/3 to 1/2. Reference: NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1, Jan, 2001

7-8

IRON SUPPLEMENTS There are a variety of iron supplements, many of which have added nutrients which may not be appropriate or needed in CKD patients. This list is not all inclusive. It contains iron compounds that do not contain added nutrients. Iron Source

O R A L

Ferrous Gluconate Ferrous Fumarate Ferrous Sulfate Polysaccharide Heme Iron Polypeptide Iron Dextran

I V

Ferrous Sodium Gluconate Iron Sucrose

% Elemental 12%

33% 20% 30% dried 100%

Examples Fergon® Ferralet®

Elemental

Dose

Side Effects

35 mg/300 mg tablet 106 mg 116 mg 50 mg 65 mg 150 mg 150 mg 7 mg/capsule

6-7/day

GI symptoms, N & V, constipation

2/day 2/day 3-4/day 3/day 1-2/day 1-2/day 2-4/day

Same as above

InFed® DexFerrum®

50 mg/mL

100 to 1000 mg

Ferrlecit®

12.5 mg/mL

62.5 to 125 mg

Venofer®

20 mg/mL

5-10 ml, 2-3 times/wk

Hemocyte® Nephro-Fer® Slow-Fe® Feosol® Niferex 150® NuIron 150® Proferrin®

Same as above Same as above “No adverse reactions” per manufacturer. Altered/metal taste, N/V, ↓ BP, flushing, myalgia/arthralgia, rash, urticaria/anaphalaxis/tachycardia Rarely-hypotension, flushing, cramps, N/V, malaise, agitation, fatigue. No reported deaths. Hypotension, cramps/leg cramps, nausea

Reference: NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1, Jan, 2001 Saunders Nursing Drug Handbook, 1999, WB Saunders Company 7-9

REASONS FOR INADEQUATE RESPONSE TO EPO THERAPY Inflammation/Infection (access, surgical inflammation, AIDS) Iron deficiency/Inadequate EPO dose Folic acid/B12 deficiency* Aluminum toxicity Malnutrition Significant chronic blood loss Hemolysis/shortened erythrocyte survival Multiple myeloma Osteitis fibrosa Hemoglobinopathies (Sickle cell disease) Angiotensin-converting enzyme inhibitors (potential) *It may be prudent to monitor folic acid and B12 levels on a regular basis. Reference: NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1, Jan, 2001

7-10

Chapter 8: BONE METABOLISM AND DISEASE IN CKD/ UROLITHIASIS

MANAGEMENT OF OSTEODYSTROPHY IN CHRONIC KIDNEY DISEASE It has been suggested that one cannot be dogmatic in the management of osteodystrophy in CKD. Therapeutic approaches must be tailored to meet individual needs and parallel constant changes in dialytic therapy. Osteodystrophy in CKD is a complex disorder of bone and mineral metabolism where correction of one abnormality can often lead to the aggravation of another. A number of protocols have been developed for the management (prevention and treatment) of bone disease in CKD. Protocols must be updated on a regular basis and reflect the changing profiles of CKD-related bone disease as well as current research. In addition, patient responses must be monitored to guide changes in protocols and ensure the best possible outcomes. Historically, each new bone disease therapy that has evolved in CKD has created new problems. From aluminum toxicity to hypercalcemia to soft tissue calcification, the quest for balance in the area of minerals and CKD-related bone disease continues. Bone and mineral abnormalitites in CKD include: hypocalemia, secondary hyperparathyroidism, hyperphosphatemia, defective absorption of calcium from the gut, abnormal bone mineral content, altered vitamin D metabolism, bone disease, soft tissue calcification, altered kidney handling of calcium/phosphorus/magnesium, pruritus, proximal myopathy, skin ulceration, and soft tissue necrosis. Risk factors that can impact the type of bone lesion include: prolonged aluminum exposure, glucocorticoid therapy, DM, beta-2 microglobulinemia amyloidosis, metabolic acidosis, hypophosphatemia secondary to aggressive dietary or binder control, or chronic low intake. The K/DOQI Bone Metabolism and Disease Work Group is developing practice guidelines for the management of bone disease in CKD. These guidelines, scheduled to be published in 2002, will objectively and critically elicit an evidence-based approach to bone disease in CKD. Watch for these guidelines from the National Kidney Foundation to update your knowledge on the topic of this chapter.

8-2

OSTEODYSTROPHY IN CKD: TYPES AND CHARACTERISTICS Type

HYPERPARATHYROID Early

HYPERPARATHYROID Late ADYNAMIC OR APLASTIC

MIXED UREMIC OSTEOMALACIA

Attributes

Excess PTH, high bone turnover, osteitis fibrosa As above

Low bone turnover PTH Oversuppression may play role Combination of mixed signs Low bone turnover

Incidence

Usual Lab Profile Alk PTH Phos M-↑ ↑

AL++

Response to Calcitriol

Ca++

P

Common

↓

↑

Less common

↑

↑

↑

↑↑

N

Nonaluminum related common, aluminum related rare Increasingly rare

N-↑

N↑

N-↓

N-↓ <100 pg/mL

N-↑

Poor, can aggravate condition

↓

↑

M-↑

N-↑

N-↑

Increasingly rare

↑

N↓

N-↓

N-↓

N-↑

Good, if predominately hyperparathyroid Poor

N-M

Good

Varied to poor

N-Within normal limits M-moderate ↑ Increased, above normal ↓ Decreased, below normal ↑↑ Very high Reference: Antonsen JE, Sherrard DJ: Renal Osteodystrophy: Past and Present. Sem Dial 9(4):296-302, 1996 8-3

NEGATIVE EFFECTS OF HYPERPHOSPHATEMIA Removal of phosphorus (P) during hemodialysis depends on pre-dialysis serum level and dialyzer used. Phosphorus removal can range from 250-1000 mg per HD treatment. In contrast, about 250-300 mg of phosphorus is removed per day with peritoneal dialysis. An estimate of P that must be controlled by binders is equal to the amount of P absorbed (approximately 50-60% of intake) minus the amount of P removed during dialysis. Adequate dialysis delivery, moderation of dietary P and adequate binder therapy are all necessary to control serum P. Consequences of hyperphosphatemia, in addition to osteodystrophy in CKD, include: 1. 2. 3. 4. 5. 6. 7.

Contributes to the calcium x phosphorus product, metastatic calcifications, and calciphylaxis. Combines with low calcium as a stimulant to PTH secretion; impairs the feedback inhibition of PTH production and secretion. Suppresses the effect of phosphate loading on renal tubular production of calcitriol. Inhibits the action of 1-alphahydroxylase and, thereby, decreases Vitamin D activation in the kidneys. Stimulates PTH secretion/parathyroid gland hyperplasia. Induces resistance to calcitriol (PTH reduction) when a serum P >8 mg/dL . Contributes to myocardial fibrosis, heart, and valve calcification, as well as cardiovascular sudden death.

HYPERPHOSPHATEMIA DUE TO RELEASE OF PHOSPHORUS FROM BONE As much as 300 mg of phosphorus per day can be released from the bone in severe hyperparathyroid bone disease. P (released directly into the blood) is not accessible to phosphate binders in the gut. The following may indicate that high serum P is, at least in part, due to release of P from the bone: 1. 2. 3.

The patient is compliant with binders and tending toward hypercalcemia with minimal or no calcium load. The PTH has been elevated for a significant time and/or there are signs of increased bone resorption. The patient is getting a significant dose of vitamin D or analog without response.

References: Daugirdas JT, Ing TS: Handbook of Dialysis, Little, Brown and Co., 1994 Antonsen J, Sherrard D: Renal Osteodystrophy: Past and Present. Sem Dial 9(4):296-302, 1996 Block GA, Port FK: Re-evaluation of Risks Associated with Hyperphosphatemia and Hyperparathyroidism in Dialysis Patients: Recommendations for Change in Management. Am J Kidney Dis 35:1226-1237, 2000 8-4

PHOSPHORUS DENSITY OF COMMON FOODS Food Beans, Dried Beer Chocolate Coffee, Brewed Cola Egg Cheese, Cheddar Cheese, Cottage Cheese, Cream Fish Liver, Beef Milk Nuts Peanut Butter Pork, Poultry Oysters Red Meats Shellfish Soybeans, Boiled Soybeans, Roasted Sunflower Seeds Tofu Yogurt

Measure 1 cup 12 oz 1 miniature 1 cup 12 oz 1 large 1 oz 1 cup 2T 3 oz 3 oz 1 cup 1 oz 2T 3 oz 3 oz 3 oz 3 oz 1 cup 1 cup 1 oz 100 gm 4 oz.

Phos (mg) 209-251 43 95 2.3 44 86 145 151-297 30 214-282 392 209-247 98-147 101-118 146-210 196 189-203 116-175 421 624 322 52-76 162-177

Pro (gm) 14-16 1 3 0 0 6 7 14-28 2 21-23 23 8 4-8 8 22-28 13 22-25 17-19 29 61 6 4-6 6

mg Phos/gm Pro 14.9-15.7 43 31.7 14.3 20.7 10.6-10.8 15.0 10.2-12.3 17 26.1-30.9 18.4-24.5 12.6-14.8 6.6-7.6 15.1 8.1-8.6 6.8-9.2 14.5 10.2 53.7 12.7 - 13.6 27-29.5

Note: If dairy products, nuts, beans, and seeds are eliminated, average mg P per gm of protein is approximately 10 to 11. Reference: US Department of Agricultrue, Agriculture Research Service, 2001. USDA Nutrient Database for Standard Reference, Release 14, Nutrient Data Laboratory Home Page, http://www.nal.usda.gov/fnic/foodcomp

8-5:

8-5

PHOSPHATE BINDING AND CALCIUM SUPPLEMENTATION Any product used for phosphate binding should be taken with meals for optimum binding. Calcium products meant to be used as a calcium supplement should be taken between meals. The K/DOQI bone disease work group is evaluating the literature regarding calcium supplementation and calcium load. Their findings are not available for this edition of the Pocket Guide, however, there is an increasing trend toward maintaining low normal serum calcium and lower calcium times phosphorus product. It has been strongly suggested that efforts to reduce PTH with high calcium levels should be abandoned. These changes in practice should be kept in mind when recommending the dose and source of phosphate binders. Iron supplements should NOT be taken with binders or calcium supplements (limits iron absorption and reduces the binding of phosphorus). Below are steps to phosphorus control: 1. 2.

3. 4. 5. 6. 7. 8. 9.

Limit dietary P as much as possible within adequate protein levels. Evaluate patient for calcium load and calcium status. Current opinion suggests that we must take care in dosing binders so that we do not add to the risk of soft tissue calcification (<2000 mg elemental Ca++/day). If serum Ca++ >9.5 mg/dL, consider adding or substituting a non-aluminum, non-calcium binder. Evaluate the actual P intake to plan the initial and subsequent binder doses. Titrate the binder dose to the meal or snack. Recommend taking binders during or immediately before or after meals. Some research indicates it may help to take binders regardless of timing, if forgotten at meal time; however, this could increase calcium absorption. Prescribe binders with consideration of medical needs, serum chemistries (including Ca x P product), patient preference for source and form as well as efficacy, availability, and cost. Use the most concentrated form and check compliance before increasing the dose. Consider binder change if source or form of binder isn’t tolerated, results are unsatisfactory, or other problems are created or exacerbated (like hypercalcemia and soft tissue calcification). Avoid aluminum-containing binders unless all other therapies fail. Limit the use of aluminum to minimal, short term dosing in patients with uncontrolled hyperphosphatemia. Do not use aluminum and citrate together.

8-6

CALCIUM COMPOUNDS % Elemental Ca++ 25% 40% 22% 9% 6.5%

Source Calcium Acetate* Calcium Carbonate** Calcium Citrate*** Calcium Gluconate Calcium Glubionate

mg Ca++/g Compound 250 400 220 90 66

*Estimated in vitro binding power: 40-60 mg P bound per 1 gram calcium acetate Reference: Slatopolsky E: Kidney International 27:173, 1985

**Estimated in vitro binding power: 39 mg P bound per 1 gram of calcium carbonate Reference: Schiller L: N Engl J Med 320:1110-1113, 1989

POTENTIAL SIDE EFFECTS OF CALCIUM-BASED BINDERS/SUPPLEMENTS: 1. Hypercalcemia (symptoms page 8-17). 2. Added calcium load (varies by compound) that can elevate Ca x P product and increase the risk for metastatic calcification. 3. GI intolerance (bloating, gas, nausea, vomiting, constipation). 4. May be limited by hypercalcemia (>9.5-10.2 mg/dL) or high calcium x phosphorus product (>55 mg2/dL2). 5. Calcium citrate is not recommended because it enhances aluminum absorption, especially when combined with aluminum-based binders.*** 8-7

COMMON NAME BRAND CALCIUM-BASED BINDERS/SUPPLEMENTS Compound Calcium Acetate Calcium Acetate Calcium Carbonate

Name Brands PhosLo

Compound 667 mg

Elemental Ca++ 169 mg

Manufacturer Braintree Laboratories

Hil-Cal

670 mg

170 mg

Hillstad (Calcium Supplement)

Calci-Chew Calci-Mix Caltrate 600 Chooz (Gum) Nephro-Calci Oscal 500 TUMS TUMS E-X TUMS Ultra TUMS 500

1250 mg 1250 mg 1500 mg 500 mg 1500 mg 1250 mg 500 mg 750 mg 1000 mg 1250 mg

500 mg 500 mg 600 mg 200 mg 600 mg 500 mg 200 mg 300 mg 400 mg 500 mg

Watson Pharmaceuticals Watson Pharmaceuticals Whitehall-Robins Schering-Plough Watson Pharmaceuticals Whitehall-Robins Glaxo Smith Kline Glaxo Smith Kline Glaxo Smith Kline Glaxo Smith Kline

Combination Binders with Calcium Mg/Ca++ Product Magnesium MagneBind™ carbonate combined 200 with calcium acetate. Magnesium is MagneBind™ dialyzable. 300 References:

Composition/ 1 Tab 200 magnesium carbonate 450 calcium acetate 300 magnesium carbonate 300 calcium acetate

Elemental Mg = 57 mg Ca++= 113 mg Mg = 85 mg Ca++= 76 mg

Manufacturer Nephro-Tech

Saunders Nursing Drug Handbook, WB Saunders, 1999 Internet: Manufacturers’ Web Sites, 2001

8-8

OTHER PHOSPHATE BINDERS Calcium-free/Aluminum-free Binders

These binders are indicated for reduction of serum phosphorus in CKD without the addition of a calcium load. They can help prevent or correct hypercalcemia, elevations of calcium x phosphorus product, and the risk for soft tissue calcification. These binders also reduce total and LDL cholesterol, and may increase HDL cholesterol. Reported side effects are minimal, primarily GI distress such as nausea, constipation, diarrhea, bloating, and indigestion. Compound Sevelamer hydrochloride

Name Brand Renagel®

Description Ca++- free, aluminum-free cationic polymer; not absorbed

Forms Renagel® Tablets 400/800 mg Renagel® Capsules 403 mg

Manufacturer Genzyme

Aluminum-based Binders Not appropriate for long term therapy but can be used (<4 weeks) in patients with significant hyperphosphatemia (>7.0 mg/dL) and when other methods of phosphate control fail. Avoid doses >2.5 gm aluminum hydroxide per day and any source of citrate. Common side effect include constipation, potential for other toxic side effects if used excessively or for long periods of time. Long term side effects can include CNS (dementia, encephalopathy) and bone effects (aluminum bone disease/osteomalacia); bone mineralization may also be impaired due to aluminum deposition. Compound Aluminum Carbonate Aluminum Hydroxide (In vitro binding power is estimated to be: 22 mg P bound per 5 ml liquid, 15 mg P bound per tablet). Balsa RW Nephron 45:16-21, 1987

Name Brands Baseljel

Form

Manufacturer

Liquid

Axcan Pharma, Inc.

AlternaGEL Alu-Cap Alu-Tab Amphojel

Liquid Capsule Tablet Liquid

Johnson & Johnson, Merck 3M Pharmaceuticals 3M Pharmaceuticals Axcan Pharma, Inc.

References: Internet, Manufacturers’ Information, 2001 8-9

AVAILABLE VITAMIN D AND VITAMIN D ANALOGS – ORAL/IV Product Calcijex® (calcitriol)* Hectorol® (doxer calciferol)

Rocaltrol® (calcitriol)

Zemplar® (paricalcitol)

Source Calcitriol, synthetic vitamin D3 Active Vitamin D hormone Prohormone metabolized in the liver to 1∝25-(OH)2 D2 and 1∝24(OH)2 D2 Not active at ingestion or injection/activated in liver Synthetic vitamin D3 1,25-dihydroxyvitamin D3 Active Vitamin D hormone

Paricalcitol sodium, synthetic-vitamin D2 analog; Active Vitamin D hormone

Forms IV

Peak Rapidly available, 3-5 day pharmacologic activity 11-12 hrs (Half life is 32-37 hours)

Action Sites Intestine, bone, kidney, and parathyroid Intestine, bone, and parathyroid

Manufacturer Abbott Labs

Oral

3-6 hours following 0.25-1mcg dose

Intestine, bone; acts on parathyroid and intestinal tissue

Roche Pharm.

IV

5 minutes, decreases within 2 hours. Halflife is about 15 hrs

Parathyroid gland, bone

Abbott Labs

IV, Oral

Bone Care Intl.

*Generic calcitriol is also available.

8-10

USE OF ACTIVE VITAMIN D OR VITAMIN D ANALOGS - ORAL/IV Parameters Serum Ca++, Adjusted* (formula pg. 8-16) Serum P Ca-P Product Serum iPTH (intact parathyroid hormone) Aluminum Bone Disease Alkaline Phosphatase

Criteria for Initiation Therapy Goals Common Monitoring* Low normal (8.5-9.5 Weekly to monthly WNL* Prevent hypercalcemia/ mg/dL)* soft tissue calcification (WNL for CKD, no dialysis) 3.5 - 5.5 mg/dL* Weekly to monthly Prevent soft tissue calcification ≤ 5.5 mg/dL* (3.5-5.5 Weekly to monthly ↓ freq. when 2-3x upper non-uremic normal; mg/dL) stable At least quarterly ↓ PTH/bone demineralization* ≤ 55 mg2/dL2* Normal bone mineralization ≥ 300 pg/mL* Aluminum, biannually WNL * (Signif. drop toward (2nd gen. iPTH) normal=potential for hyper Ca+) Monthly Absent* ΝΑ Steps to Initiation: (* Acceptable values may vary by facility/MD. Ca++, P, and product targets may be liberalized slightly with higher iPTH) 1. Obtain baseline chemistries including iPTH and stop other Vitamin D forms. 2. Control serum P to <5.5 mg/dL*; adjust binders and/or dietary intake. (might consider up to 6.5 mg/dl if PTH very high) 3. Control serum calcium to WNL* or ≤9.5 mg/dL (adjust oral intake and/or dialysate level). 4. See manufacturer’s information for dosing guidelines; most recommend higher initial doses for higher iPTH. 5. Monitor response/trends. Change dose accordingly based on iPTH/Ca++/P/product/alkaline phosphatase; allow adequate time for physiologic response before changing. Monitor Ca++/P/product at least weekly w/ dose changes. 6. Modify dose, hold, or discontinue Vitamin D/analog if Ca x P product >55 mg2/dL2*, Ca++> normal*, P ≥5.5 mg/dL*, PTH ≤ 100 pg/mL. 7. Restart when above values are within desired levels. If held for hypercalcemia or low PTH, restart at lower dose. If held for hyperphosphatemia or high product, counsel patient on diet/binders, continue same dose or decrease. References: Coburn J: Calcitriol in the Management of Renal Osteodystrophy. Sem Dial 9(4):316-326, 1996 Kates D: Control of Hyperphosphatemia in CRF: Role of Aluminum. Sem Dial 9(4):310-315, 1994 Block GA, Port FK: Re-Evaluation of Risks Associated with Hyperphosphatemia and Hyperparathyroidism: Recommendations for a Change in Management. Am J Kidney Dis 35(6):1226-1237, 2000 8-11

PROTOCOLS FOR THE ADMINISTRATION OF VITAMIN D AND VITAMIN D ANALOGS There is considerable variation in the definition and treatment of osteodystrophy in CKD which, in part, stimulated the convening of the NKF K/DOQI Work Group for Bone Metabolism and Disease. The clinical practice guidelines for bone metabolism and disease are being developed and will provide evidence-based recommendations. As with the other K/DOQI guidelines, clinicians are encouraged to review and implement the recommendations as appropriate to individual clinical practice and the needs of their patients. Assessment, monitoring and treatment of abnormal bone metabolism in CKD lends itself to care maps or protocols. Protocols should: 1. 2 3. 4.

Promote patient safety and incorporate strategies with the fewest side effects. Be consistent with current, valid research, and be regularly updated to reflect changes in research. Reflect the care team consensus for management of bone disease in CKD (or other problems). Provide a schedule for changes (dose, medication, and method of administration) that allows time for the effect of therapy to be observed. 5. Be logical and easy to follow, minimize paperwork, and allow for timely, appropriate interventions. 6. Include a mechanism to inform the patient of his/her role and progress. 7. Define limits that allow the physician to delegate tasks to other members of the care team. 8. Return responsibility for monitoring and administering patient care to the physician when requested/needed therapies exceed the protocol limits. 9. Identify outcome measures and provide tracking mechanisms. Tracking outcomes provide guidance for appropriate changes in protocols to ensure continuous improvement of outcomes. 10. Provide regular assessment and revision of protocols in light of facility needs or limitations and patient outcomes.

8-12

MANUFACTURERS’ SUGGESTED DOSING FOR VITAMIN D OR ANALOGS PTH Level Initial dose

Calcijex® 0.2 mcg/kg 3 x wk (1-2 up to 4 mcg)

Zemplar® 0.04 - 0.1 mcg/kg 3 x wk (2.8-7 mcg)

Rocaltrol® 0.25 mcg/day Most dialysis pts need 0.5-1 mcg/d

Hectorol® IV 4 mcg 3x week if PTH >400 pg/mL

Hectorol® Caps 10 mcg 3x week if PTH >400 pg/mL

Other miscellaneous information

Initial from 0.5 – 4 mcg 3x wk 2-4 week intervals

Shown safe up to 0.24 mcg/kg or 16.8 mcg 2-4 week intervals

Capsule (0.25/0.5 mcg ) Oral solution: 1mcg/mL

Administer 3 x wk at the end of dialysis

Soft gelatin capsules, 2.5 mcg

4-8 week intervals

8 week intervals

8 week intervals

Usual dose change PTH same high or ↑ Decreasing by <30%

0.5 – 1 mcg Increase dose

2 – 4 mcg Increase dose

0.25 mcg Not noted

1 – 2 mcg Increase dose

2.5 mcg Increase dose

Increase dose

Increase dose

Not noted

PTH: <50% decrease, ↑ dose by 1-2 mcg

Decreasing ≥30 <60%

Maintain dose

Maintain dose

Not noted

PTH: 150-300 pg/ mL: maintain dose

PTH: <50% decr., ↑ dose by 2.5 mcg PTH: 50-300 pg /mL, maintain dose

Decreasing by ≥60%

Decrease dose

Decrease dose

Not noted

PTH: <100 hold 1 week, restart at mg lower dose

PTH in desired range

Maintain dose

Maintain dose

Maintain dose

Maintain dose

Frequency of dose changes

PTH: <100 pg/mL, hold for 1 week, restart at lower dose Maintain dose

8-13

FACTORS AFFECTING THERAPEUTIC RESPONSE TO VIT D/ANALOGS IN HYPERPARATHYROIDISM Factor Hyperphosphatemia Type of binder utilized: Aluminum gels Calcium salts Sevelamer HCL Dialysate Calcium: 3.0 to 3.5 mEq/L 2.5 mEq/L 2.0 mEq/L Parathyroid gland changes: Increased size Hyperplasia Dosing Route: Oral IV

Response To Vitamin D/Analogs Decreased

Effects/Limitations Inhibits Vitamin D production/effect

Enhanced by better control of serum P May require large doses for P control May allow more aggressive Vitamin D therapy with acceptable Ca x P product

Risk for aluminum toxicity/bone disease Risk for hypercalcemia Cost/reimbursement

May limit dose of Vitamin D/analog Allows more therapeutic Vitamin D/analog and/or binder dose May allow even higher Vitamin D doses

Increased risk for hypercalcemia Better PTH suppression, phosphorus control, less hypercalcemia Monitor for low serum levels

Diffuse, ↑ cells, but uniform Nodular glands, less response

Increased hormone production ↓ vitamin D receptors, ↓ suppression

Both good with adequate doses, depending on level of disease

Reimbursement issues for some products. Hypercalcemia/high Ca x P product.

Editor’s Note: Calcium-free, aluminum-free binders can help minimize hypercalcemia/soft tissue calcification. Reference: Coburn J, Frazao J: Calcitriol in the Management of Renal Osteodystrophy. Sems in Dial 9:316-326, 1996 8-14

MANAGEMENT OF ADYNAMIC (LOW TURNOVER) BONE DISEASE 1. Aluminum Bone Disease - generally symptomatic (bone pain, myopathy, pathologic fractures). 2. Non-aluminum Aplastic Bone Disease - because of hypercalcemia, may have increased risk for extra-skeletal calcifications, but generally are not very symptomatic. Risk factors include peritoneal dialysis with high calcium solutions, use of calcium based binders, presence of diabetes mellitus, advanced age, and vitamin D treatment. 3. Diagnosis: iPTH of <100-150 pg/mL is associated with a higher incidence of low turnover bone disorder. “Normal” PTH levels are not “normal” for renal patients.

Management Serial monitoring of iPTH Do NOT routinely order Vitamin D for all patients. Initiation should be based on iPTH levels specific to unit or physician parameters or when iPTH is >300 pg/mL (original article suggests 200-400pg/mL). If iPTH levels drop to <100-150 pg/mL, DC/hold Vitamin D and/or titrate the dose to maintain iPTH between 150-300 pg/mL. Avoid or limit the use of aluminum binders and other sources of aluminum. Maintain serum calcium in the lower range, which stimulate PTH secretion and help normalize bone metabolism. Usually requires decreased dialysate Ca++ levels and decreased reliance on Ca based binders. Individualize patient treatment with dialysate calcium concentration, binders, and supplements to maintain serum phosphorus, serum calcium, and iPTH levels within acceptable ranges. Editor’s Note: iPTH goals vary depending on the reference (1.5-3x upper normal, 150-300 pg/mL for PTH2 (1-84 + 7-84 fragment). PTH3 (1-84) values are approximately 50% lower than PTH2 in most patients. Target ranges and interpretation of PTH3 are still being investigated with bone biopsies to correlate bone histology with specific PTH3 values. For those who are already using PTH3, Vitamin D protocol goals could be adapted using target PTH2 values divided by two. When transitioning from PTH2 to PTH3 clinicians should pay special attention to those patients who fall out of the observed 2:1 ratio and those whose PTH values are inconsistent with bone-related clinical symptoms. Reference: Pei Y, Hercz G: Low Turnover Bone Disease in Dialysis Patients. Sems in Dial 9(4): 327-331, 1996 8-15

FORMULAS FOR ADJUSTED CALCIUM 1. Adjusted serum calcium = measured total calcium + 0.0176 (34 - serum albumin (g/dL)) Reference: Fernandez E, Montoliu J. Successful treatment of massive uremic tumoral calcinosis with daily hemodialysis and very low calcium dialysate. Nephrol Dial Transplant 9:1207-1209, 1994. 2. Adjusted serum calcium = Total calcium mg/dL + 0.8 x (4.0 - serum albumin (g/dL)) Reference: Portale AA. Blood calcium, phosphorus, and magnesium in Primer on Metabolic Bone Diseases and Disorders of Mineral Metabolism, Ed. Favus MJ. Lippincott, Williams, and Wilkins, Philadelphia, 1999, pp 115-118. There are a number of different formulas that correct serum calcium for low albumin or low total protein. Formula 1 above was derived in a study employing good statistical methods and strict control of blood processing. This formula had an interclass correlation value of 0.84 and most closely approximates total calcium in patients with CKD. Formula 2 is a commonly used, simplified formula for adjustment total calcium for changes in plasma albumin. It is accepted that total calcium needs to be adjusted for the level of albumin to better reflect free calcium. Symptoms of hypercalcemia have been observed in hypoalbuminemic CKD patients with high normal serum calcium levels. If adjustment results are questioned, one should perform an ionized calcium measurement. IONIZED CALCIUM CALCULATION Ionized calcium in mg/dL = (Total serum Ca++ mg/dL X 6) - (Total Protein/3) (1) Total protein + 6 Ionized calcium in mg/dL = 1- (8 X albumin) + (2 X globulin) + (3 X unadjusted serum calcium) (2) (where globulin = total protein - albumin) References: 1 Raphael SS: Lynch’s Medical Laboratory Technology, 4th Ed, W.B. Saunders, 1983 2 Kaminsky M: (Ed) Hyperalimentation: A Guide for Clinicians, Dekker, Inc., NY, 1985 8-16

SYMPTOMS OF HYPERCALCEMIA AND HYPOCALCEMIA Hypercalcemia: MildEarly Stage

May be asymptomatic. Weakness, headache, nausea, somnolence or irritability, vomiting, dry mouth, constipation, muscle pain, metallic taste, shortened Q-T interval on EKG, abnormal U waves

Severe - Late Stage Elevated BUN & SGOT/SGPT, pruritus, hypertension, anorexia, weight loss, calcific conjunctivitis, pancreatitis, mental confusion, overt psychosis, cardiac arrhythmias, sensitivity to light, rhinorrhea, polydipsia, hyperthermia Hypocalcemia: Mild - Early Stage Severe - Late Stage

May be asymptomatic. Prolonged Q-T interval, EKG T wave may be lower/inverted Tetany, numbness/tingling progressing to muscle spasm and seizure

ETIOLOGY OF HYPERCALCEMIA Absorptive Pharmacological doses of active Vitamin D Large doses of calcium (supplements, binders, foods, dialysate)

Resorptive Primary hyperparathyroidism Malignant neoplasms Vitamin D intoxication, excessive Vitamin A Prolonged immobilization Adrenal insufficiency/Hyperthyroidism

References: The Merck Manual of Diagnosis and Therapy, 13th Edition, Rahway, NJ, 1977 Tisher C, Wilcox C: Nephrology for the House Officer, Williams & Wilkins, 1993

8-17

POTENTIAL INDICATIONS FOR PARATHYROIDECTOMY While treatment with Vitamin D/analogs has substantially improved the course of secondary hyperparathyroidism, the need for parathyroidectomy still exists in certain clinical situations. The list below outlines some of the conditions which may indicate the need for consideration of parathyroidectomy. 1. Hypercalcemia, resistant to medical therapy and/or in the presence of bone erosions, marked elevations of parathyroid hormone, and bone biopsy results demonstrating osteitis fibrosa. 2. Ischemic skin ulcerations associated with vascular calcifications or calciphylaxis. Extensive vessel calcifications without symptoms may NOT absolutely indicate the need for a parathyroidectomy since some research has shown that the calcification progresses even after parathyroidectomy is performed. 3. Extremely severe, unresolving pruritus in the presence of significantly elevated iPTH. 4. Persistent hyperphosphatemia unresponsive to medical therapy. 5. PTH is considered to be a uremic toxin which may cause adverse effects such as bone marrow dysfunction (anemia), myocardial dysfunction (congestive heart failure), and neuromuscular problems (peripheral neuropathy). Such toxic effects may be considered indications for parathyroidectomy, but without proof of a clear, direct relationship, these problems should not be the sole reason for recommending parathyroidectomy. 6. Severe hyperparathyroidism resistant to medical therapy. (i.e. iPTH > 800 pg/mL). Reference: Llach F, Nikakhtar B: Parathyroidectomy in Dialysis Patients: Indications, Surgical Approach, Complications, and Clinical Management. Sems in Dial 9(4):332-338, 1996

8-18

COMMON CLINICAL COURSE AFTER PARATHYROIDECTOMY Time Immediate post-op and up to one year

~Day 2 post-op to months after surgery

~Day 4 post-op

Clinical Course Hypophosphatemia (more profound in patients with higher PTH and plasma alkaline phosphatase) secondary to decreased mobilization of P from bone and/or increased movement into bone. Significant, precipitous decline (as much as 60%) in serum calcium which may be accompanied by numbness, paresthesia, and tetany. The decline is correlated with the severity of hyperparathyroidism. An insignificant drop in calcium suggests that too much of the gland was left or bone pathology was not severe (osteitis fibrosa). A marked increase in alkaline phosphatase (peak 7-14 days) with an increase in osteoblastic activity, then decline typically begins by week 3 and may reach normal after 6 months.

Intervention Serum P should be maintained at 3.5 to 5.0 mg/dL. Oral calcitriol is generally most effective in correcting hypocalcemia and hypophosphatemia. Large doses of oral or IV calcium are always needed to correct hypocalcemia. Increase daily doses from 0.5 to 1 gm at an interval of 3 to 7 days until serum calcium begins to rise. Give IV calcium with corrected serum level <7.5 mg/dL or tetany. Prompt post-op use of calcitriol enhances calcium absorption/bone formation. All laboratory parameters of bone health should be carefully and regularly monitored.

Reference: Llach F, Nikakhtar B: Parathyroidectomy in Dialysis Patients: Indications, Surgical Approach, Complications, and Clinical Management. Sems in Dialysis 9(4):332-338, 1996

8-19

UROLITHIASIS (NEPHROLITHIASIS/KIDNEY STONES) Urolithiasis is the presence of calculi in the urinary tract. The male-to-female incidence ratio is 4:1, with 240,000 to 720,000 Americans affected yearly. Eighty percent of calculi are composed of calcium (either oxalate or phosphate), with others composed of struvite, uric acid, or cystine. Type of stone indicates cause: 1. Calcium type I—increased small bowel absorption of calcium unrelated to intake 2. Calcium type II—increased dietary calcium intake 3. Calcium type III—increased vitamin D synthesis 4. Calcium oxalate-idiopathic/primary intestinal disorders, chronic diarrhea with inflammatory bowel or steatorrhea 5. Struvite (magnesium ammonium phosphate)-mainly women, due to infection with urease-producing organisms 6. Uric acid—metabolic defects or dietary excess of uric acid; bowel disease or chemotherapy 7. Cystine-due to chronic diarrhea, type I renal tubular acidosis, chronic hydrochlorothiazide treatment Risk Factors Excess intake of calcium, oxalate, or purines in predisposed individuals Inadequate fluid intake Sedentary occupation Area of high humidity, elevated temperatures (summer) Hyperparathyroidism Renal tubule defects (renal tubule acidosis) Bowel disease or ileal bypass for obesity Genetics-cystinuria, an autosomal recessive disorder (markedly increased cystine excretion) Excessive intake of certain vitamins and minerals Gout Use of certain diuretics 8-20

TREATMENT OF CALCIUM STONES Nutrient Calcium

Sodium Protein Phosphorus Fluid Vitamins C & D Oxalate

Recommendation Children: RDA for age/gender Adult men/women: 800 mg/day Pregnant/lactating women: 1200 mg/day Post-menopausal women: 1200-1500 mg/day 100-150 mEq sodium/day Children: RDA for age/gender/treatment modality Adults: 1 gm/kg Unrestricted Children: Unrestricted, high intake encouraged Adults: > 2 L/day Avoid levels above RDA Limit dietary sources, especially nuts/chocolate

Diet is used as first line treatment and in conjunction with drug therapy. References: See next page.

8-21

HYPEROXALURIA The most common cause of hyperoxaluria is intestinal disease with increased oxalate absorption. It is rarely caused by a metabolic abnormality that results in the body producing too much oxalate. Type Hyperoxaluria

Cause Increased excretion in urine due to excessive absorption of dietary oxalate

Dietary oxalate: Protein: Adults: Children: Fat: Calcium: Vitamin C or D Fluid: Adults: Children:

Dietary Treatment <40-50 mg/day 1 gm/kg RDA for age/gender <30% of total calories/day <1 gm/day, if MD ordered Limit to RDA >2 L/day Unrestricted, high intake encouraged

References: Brzezinski E et al: Oxalate Content of Selected Foods. UC, San Diego, 1996 Laumann E et al: Management of primary hyperoxaluria: efficiency of oral citrate administration. Ped Nephrol 7:207, 1993 Massey L et al: Effect of dietary oxalate and calcium on urinary oxalate and risk of formation of calcium oxalate kidney stones. J Am Dietetic Assoc 903(8):901, 1993 Ono K: Secondary hyperoxalemia caused by vitamin C supplementation in regular hemodialysis patients. Clin Nephrol 26(5):239-243, 1986 Polinsky M et al: Renal Stones: Hypercalcuria. Advances in Pediatrics, Vol 49, 1993 Smith CL et al: Dietary Factors in Calcium Nephrolithiasis. JRN 2:146-153, 1992 Wendland B: Nutrition management of the patient with urolithiasis. In: Stover, J., Ed. A Clinical Guide to Nutrition Care in End Stage Renal Disease. ADA, 1994 8-22

OXALATE CONTENT OF COMMON FOODS Low <2 mg/serving MEATS/SUB: Eggs, cheese, lean meats, seafood VEGETABLES: Avocado, broccoli, cabbage, potato, radish, turnips, water-chestnuts, mustard greens FRUITS: Banana, cherries, cranberries-canned, green seedless grapes, lemon/lime juice, mangos, melons, nectarines, peaches-Hiley canned, pineapple, plumsgreen/Golden age, pears-Bartlett canned, orange juice, papaya, strawberries-fresh. STARCHES: Barley, cornflakes, macaroni, rice/wild rice, noodles, oatmeal, white bread FATS: Mayonnaise, salad dressing, vegetable oils, butter, margarine MISCELLANEOUS: Jams, jellies from fruit listed above, sugar, honey, corn syrup, unflavored gelatin, maple syrup, vanilla extract, vinegar, cornstarch, salt, pepper <1 tsp/day

Medium 2-10 mg/serving MEATS/SUB: Sardines, bacon VEGETABLES: Asparagus, carrots-canned, cauliflower, corn, cucumber, onions, peas, lettuce, dandelion greens, eggplant, escarole, kale, parsnips, lima beans, tomato, mushrooms FRUITS: Apple, apricots, black currants, cranberries-dried, grapefruit, orange, peaches-Alberta, pears - raw, plums-stewed, prunesItalian, pineapple-Dole, coconut, kiwi STARCHES: Cornbread, sponge cake, spaghetti in tomato sauce, cornmeal, Cheerios®, bagel, brown rice, garbanzo beans-canned, lentils, split peas, macaroni, spaghetti, corn tortilla, English muffin, whole wheat bread MISCELLANEOUS: Vegetable/ tomato soup, tofu-firm, malt, mustard-Dijon, ginger-raw

High >10 mg/serving MEATS/SUB: Baked beans in tomato sauce, peanut butter, soybean curd (tofu) VEGETABLES: Beans - boiled or raw, beets, celery, Swiss chard, chives, collards, leeks, mustard greens, okra, peppers, sweet potato, rutabaga, spinach, summer squash, watercress FRUITS: Berries, concord grapes, red currants, fruit cocktail, gooseberries, lemon/orange peel, raspberries, rhubarb, strawberries-canned, tangerine, plumsDamson STARCHES: Fruitcake, grits, soybean/graham crackers, wheat germ, fig cookies, popcorn, whole wheat flour FATS: Nuts - peanuts/pecans, sunflower seeds, mayonnaise-Heinz MISCELLANEOUS: Chocolate, dry cocoa, pepper in excess of 1 tsp/day, cinnamon, marmalade, jellies from fruits listed above.

Reference: Brzezinski E at al: Oxalate Content of Selected Foods. Clinical Research Center, UCSD Med Center, 1996 8-23

SOFT TISSUE CALCIFICATION AND CALCIFIC UREMIC ARTERIOPATHY (CALCIPHYLAXIS) Factors that may predispose CKD patients to soft tissue calcification: High calcium x phosphorus product An increase in local tissue pH Secondary hyperparathyroidism Local tissue injury Dialysis removal of calcification inhibitors A high calcium x phosphorus product in the extracellular fluid is probably the most pathogenic factor but the exact calcium x phosphorus level at which soft tissue calcification begins is not absolutely known. The current literature supports maintaining the calcium x phosphorus product in the range of 55 or below because of other contributing factors and the differences in the chemical nature of soft tissue calcification. Dietitians can help monitor for vascular calcification during monthly visits and/or during physical exams (especially in diabetics): Long term hyperphosphatemia? Significant calcium load? Calcium can be normal or elevated Lesions may be preceded or accompanied by severe pain Before a lesion appears, there may be tender, subcutaneous nodules or blotchy, bluish discoloration Raynaud’s disease (gangrene phenomenon) may also precede lesions on the fingers or toes Ulcers usually develop slowly over several months; skin or muscle necrosis may appear and progress rapidly Calcific uremic arteriopathy (calciphylaxis) can be life-threatening and must be treated early and aggressively. References: Goodman WG, Goldin J, Kuizon BD, et al. Coronary artery calcification in young adults with ESRD undergoing dialysis. N Eng J Med 342(20):1478-1483, 2000 Kimura K, Saika Y, Otani H, et al. Factors associated with calcification of the abdominal aorta in HD patients. 8-24 Kidney Int (Suppl) July 71:S238-S241, 1998

Chapter 9: MALNUTRITION IN CHRONIC KIDNEY DISEASE

ADULT MALNUTRITION Type CAUSE/ DESCRIPTION

Kwashiorkor Acute protein deficiency, rapid onset/catabolic stress in a previously well-nourished pt.

Marasmus Chronic protein/energy deficit, gradual wasting, adaptive decrease in energy expenditure

Mixed Advanced protein/energy deficit superimposed with increased protein needs or losses

ANTHROPOMETRY

Less wasting of muscle stores, less weight loss than marasmus due to rapid onset Serum proteins are generally low, diagnosis with albumin <3 g/dL, altered electrolyte state

Diminished fat and muscle stores, growth retardation in children Serum proteins are preserved initially by recycling of aa and ↓ urea synthesis

Rapid depression of fat and muscle stores

OTHER SIGNS

Characterized by pitting, painless edema to extremities, notable skin lesions/peeling

Nutrition-related edema is not present, levels of insulin and thyroid hormone are ↓

Notable edema, wasting and multiple organ system deterioration

INTERVENTION

Supplement with fluids, electrolytes, vitamins, minerals, protein as indicated

Calories and protein orally; aggressive support if weight is ↓ by 20-30%

Prompt feeding (enteral or parenteral or both) to avoid mortality

LAB

Serum visceral proteins are very depressed

Reference: Simko MD: Nutritional Assessment: A Comprehensive Guide for Planning Intervention, ASPEN, 1995

9-2

FACTORS THAT CAN CAUSE OR EXACERBATE MALNUTRITION IN CHRONIC KIDNEY DISEASE 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Increased needs and additional losses Abnormal metabolism, absorption, or utilization of nutrients Inadequate dialysis treatment Anorexia, inappropriate or poor intake Excessive dietary restriction Psychosocial problems Superimposed illness Catabolism of dialysis (including bioincompatible membranes) Endocrine disorders Acidosis

Reference: Kopple JD, Massry S, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997

9-3

EVALUATION OF WEIGHT LOSS OVER TIME

Time 1 Week 1 Month 3 Months 6 Months

Significant Loss Severe Loss 1% >1% 5% >5% 7% >7% 10% >10% Other Indications for Risk of Malnutrition Oral intake compromised for >2 weeks Extensive nutrient loss for >1 week Weight < 95 % of usual/standard weight (See page 1-18) BUN < 40 mg/dL (in dialysis patients) Cholesterol <150-180 mg/dL Body Mass Index < 20 (See page 1-20 & 21) (Dialysis M:23.6 F:24) Recent hospitalization Chronic acidosis/serum bicarbonate < 22 mEq/L

Note: SGA rates any weight change (within 6 months) of +/− 5% as normal, loss of > 5% to 10% as significant for mild to moderate malnutrition, and a weight change of >10% as significant for severe malnutrition. Values in italics signify K/DOQI recommendations. References: Page CP: Nutritional Assessment and Support: A Primer, Williams & Wilkins, 1994 Blackburn G: Nutrition & metabolic assessment of the hospitalized patient. JPEN 1:11-22, 1977 Mitch WE: Mechanisms Causing Muscle Wasting in Uremia. J Ren Nutr 6(2):75-78, 1996 NKF K/DOQI Clinical Practice Guidelines for Nutrition in CRF. Am J Kidney Dis 35 (Suppl 2), June, 2000 9-4

CRITICAL PROTEINS FOR ASSESSING MALNUTRITION

1 2

Protein Albumin*

Half Life 3 weeks

Transferrin

8 days

TBPA1

2 days

RBP 2

12 hours

Depleted Level <3.5 g/dL (depends on type of measurement/lab normals) <200 mg/dL

Body Pool 3-5 gm/kg

Limitations Slow response to depletion or repletion, altered by factors other than malnutrition

<0.1 gm/kg

<22 mg/dL (CKD < 29-30 mg/kg) <4.5 mg/dL

0.01 gm/kg

Affected by Fe++ stores Not considered a good marker in CKD patients. Not routinely performed in all facilities. TBPA is excreted by the kidneys, thus reference range is higher in CKD.

0.002 gm/kg

Thyroxine Binding Prealbumin (Transthyretin) Retinol Binding Protein

*Potential Effects of Hypoalbuminemia Alteration in GI function; promotion of gastric stasis; prolongation of bowel transit time, decreased colon resorption of salt/water, decreased absorption of food and drugs, diarrhea, cholestasis, altered intravascular oncotic pressure, and fluid balance. Potential for decreased immunity/delayed wound healing/infection and predictor of increased morbidity/mortality. Hypoalbuminemia may be a nonspecific marker of illness as well as a marker of malnutrition. Inflammation and infection can cause low serum albumin in the absence of malnutrition. References: Abstract: Gastroenterology 88:1336, 1984; and 90:1401, 1986 Page CP: Nutritional Assessment and Support: A Primer. Williams & Wilkins, 1994 Gibson RS: Principles of Nutritional Assessment, Oxford Press, 1990 9-5

GUIDELINES FOR ENTERAL FEEDING Indications for Use* Failure of intense nutrition counseling Functional GI tract Patient willingness Tolerance of fluid load Inability to meet needs w/traditional foods

Complications GI disturbance

Over/underhydration Insufficient/excess kcals or protein

Possible Solutions Dilute formula, limit volume per feeding, change formula, use lactosefree, review/change meds, decrease osmolality, stop for 8-12 hrs; restart with smaller, more frequent doses Change formula concentration and/or volume Change formula or concentration, add modular fat, CHO or protein source to tailor kcal or protein levels Modify intake of other foods, change formula, change volume

*If a patient is unable to eat, sleep, Electrolyte imbalance has poor appetite, or unexplained N & V, assess dialysis adequacy Advantages: Enteral feeding maintains gut integrity and host defenses. It is safe and less costly than IDPN, TPN. It stimulates a favorable insulin response Reference:

Page CP: Nutrition Assessment and Support: A Primer. Williams & Wilkins, 1994

9-6

ENTERAL NUTRITION SUPPLEMENTS This list of products is limited to those that could be used in CKD patients. Most basic or non-specific supplements were eliminated in the interest of space. CHO/protein/fat are in grams; sodium/potassium/phosphorus/calcium are in milligrams. PRODUCT

Amt

Kcal

CHO (gm)

PRO (gm)

Na+ (mg)

Fat (gm)

K+ (mg)

P (mg)

Ca++ (mg)

Uses

8 oz 360 200 45 350 14 200 14 200 C,V, O, S, T, HC, HP Boost Plus 8 oz 10.3 250 200 25 430 10.6 310 330 C, S, DM, F , T Choice DM C, S, F 8 oz 12 250 200 25 430 10.6 250 250 Choice HC, clear liquid 8 oz 0 300 65 65 40 10 20 60 Enlive C, O, S, HP, V 8 oz 6 225 290 31 500 12 250 300 Ensure Hi Pro C, DM, O 8 oz 11 220 210 22 370 10 250 250 Glucerna Shake C, O, T, Renal 8 oz 24.1 470 190 47 300 17.7 189 240 Magnacal Renal C, O, T, S, Renal 8 oz 22.7 475 200 52.8 250 16.6 165 325 Nepro C, HC, V, O, T, S 8 oz 24.1 475 250 47.3 192 17.4 154 308 Novasource Renal C, S 2 scp 2.8 125 210 18.8 270 6.25 480 110 NuBasics Coffee S, O 5.5 oz 0.1 163 50 34 50 6.5 166 83 NuBasic Juice S, O, 1 pkt 9.2 250 390 33.1 310 8.75 165 165 Nubasic Soup C, S, O, HP, LR, T 8 oz 8.3 250 219 28.2 312 15.6 145 145 Nubasic VHP C, S, O, HP, HC, V, T 8 oz 20 500 185 51.2 314 17.5 176 350 NutriRenal (250 ml) S 4 oz 11 250 NA 31 15 8 60 NA ReNeph S, DM 4 oz 11 230 NA 23 15 9 60 NA ReNeph No Sugar DM, F, O 8 oz 11.1 250 230 23.4 270 15 220 220 Resource Diabetic 8 oz 0 180 <70 36 <22 9.0 160 135 Resource Frt Drink C, S, O, T, V, HC 8 oz 22.7 475 185 61 265 7.1 175 330 Suplena V=volume restricted, C=complete, S=supplement to food, O=appropriate for oral, T=appropriate for tube, DM=appropriate for persons with diabetes, A=additive to other foods, HP=high protein, HC=high calorie, LR=low residue, F=added fiber, NA=information not available. Due to frequent changes, clinicians are encouraged to update the information regularly. 2-7: Reference: Internet/Manufacturers’ Product Information 9-7

SPECIALTY NUTRITION BARS/COOKIES Product Boost Bar Choice DM Bar Ensure Bar Glucerna Bar NuBasic Bar ProFortified Cookie ReNeph Cookies

Amt

Kcal

1.6 oz 1.23 oz 1 bar 1.34 oz 1 bar 1 2 oz

190 140 130 140 125 260 210

CHO (gm) 29 19 21 24 16.6 28 29

PRO (gm) 4 6 6 6 4.4 7 9

Fat (gm) 6 4.5 3 4 4.6 14 7

Na+ (mg) 90 65 115 75 135 180 NA

K+ (mg) 105 105 200 80 220 138 125

P (mg) 150 110 150 150 100 57.3 64

Ca++ (mg) 150 133 80 250 100 NA NA

Uses S,V, O DM, S, V, O C, S, V, O C, DM, F, V, O C, S, V, O S, O, V S, O, V

SPECIALTY NUTRITION PUDDINGS Product

Amt

Kcal

Boost Pudding Ensure Pudding

5 oz 5 oz

240 250

CHO (gm) 32 27

PRO (gm) 7 4

Fat (gm) 9 5

Na+ (mg) 120 240

K+ (mg) 320 330

P (mg) 200 200

Ca++ (mg) 200 200

Uses O, V, S C, S,O, V

V=volume restricted, C=complete, S=supplement to food, O=appropriate for oral, T=appropriate for tube, DM=appropriate for persons with diabetes, A=additive to other foods, HP=high protein, HC=high calorie, LR=low residue, F=added fiber, NA=information not available. Due to frequent changes, clinicians are encouraged to update the information regularly. Reference: Manufacturers’ Information

9-8

MODULAR PRODUCTS (Added to other sources of nutrition) Product

Amount

Kcal

Additions® Boost High Pro® Casec Dry® 1 ProCel® 3 Pro Mod®5 Resource® Inst. Pro 2 Vyo Whey Pro® 4 Moducal® Dry1 Polycose® Dry 5 Polycose® Liquid5 MCT Oil®1 Microlipid® 1

1 scoop 54 gm 1 Tbsp 1 scoop 6.6 gm 1 scoop 1 scoop 1 Tbsp. Per gm Per ml Per ml Per ml

100 200 17 28 28 25 82 30 3.8 2.0 7.7 4.5

1

CHO (gm) 9 36 0 <0.4 0.67 0 3 8 0.94 0.2 ---

Mead Johnson 2Novartis 3Tyler Medical Supplies Reference: Internet, Manufacturers’ Information

Pro (gm) 6 13 4 5.3 5 6 20 -----4

Nutrition

Fat (gm) 5 1 0.09 <0.5 0.6 0 1 ------

Na+ (mg) 100 190 4.4 <10 25 35 60 -<1.1 Neg. ---

K+ (mg) 3 560 Neg. <30 45 7 185 -Neg. Neg. ---

P (mg) 34 250 35 <23 33 3.5 NA -Neg. Neg. ---

Ca++ (mg) 3 290 62 <30 <30 7 NA -<0.3 Neg ---

Adds Protein Protein Protein Protein Protein Protein Protein CHO CHO CHO Fat Fat

5

Ross Products Division, Abbott Labs

9-9

ORAL AMINO ACID THERAPY Oral essential amino acid supplements are safe and effective in treating people with kidney disease. They have been successfully used to enhance the efficacy of a low protein diet in CKD (not on dialysis) and to treat hypoalbuminemia in CKD patients. They are not recommended as the sole source of nutrition. Product Aminess® Nutramine T™

Amino Acid Content Each table contains 720 mg of amino acid and 88 mg of nitrogen (= to 0.55 gm protein) 3.5 gm UPS grade amino acid in 1 packet

Form Tablets

Powder/granules to be used with foods/liquid to make chewable “candy,” custard, beverage, other foods

Manufacturer/Distributor Recip AB, Stockholm

Calwood Nutritionals, Inc.

9-10

TUBE FEEDINGS – Special Considerations for CKD 1. Moderate protein and electrolyte levels plus added fiber may be best. Too much protein can add risk for dehydration, hypernatremia, hyperchloremia, and azotemia especially in elderly and those with compromised kidney function. 2. Concentrate formulas to minimize fluid load. May need to dilute concentrated formulas at initiation. 3. Start slowly. Continuous or cyclic delivery may be tolerated best. 4 May not tolerate the free water or flush volumes suggested by manufacturers. Monitor fluid status carefully. 5. Cyclic delivery may decrease daytime fullness and allow the patient to eat at mealtimes, if physically possible. 6. Portable pumps allow easy transport to dialysis treatment. 7. Monitor chemistries (urea, electrolytes/minerals). Phosphate binders may need to be held if refeeding syndrome occurs. 8. Review formulas considering that some products may have inappropriate levels of vitamins, minerals, electrolytes, protein, calories. If renal formulations are used as the sole source of nutrition, monitor for low levels of minerals and electrolytes. 9. Monitor for diarrhea (too rapid infusion, bacterial contamination, fecal impaction, antibiotic-induced, hypoalbuminemia, malabsorption) Feeding Type Continuous

Description Pump is used to deliver feeding at a regulated rate

Intermittent

Given in specific volumes every 3 to 4 hours over a specified period of time Feeding the patient continuously via pump over only part of the day (usually 12-16 hours)

Cyclic

Advantages Reach goals more quickly Patient tolerance enhanced Nutrient absorption is maximized Mobility Less costly

Disadvantages Requires pump Difficult in disoriented patients More costly Decreased mobility Fullness, Discomfort Reflux, Staff time

Frees patient during the day May be more well tolerated than intermittent Decreased fullness Can help transition to full oral intake

Need higher hourly rate of infusion or more concentrated formula to meet needs (requires more water volume)

Reference: SpringNet, CE Connection, Internet 9-11

COMMON TUBE FEEDING SITES Site Intragastric

Nasoduodenal or Nasojejunal PEG: (Percutaneous Endoscopic Gastrostomy)

Jejunostomy

Reference:

Characteristics Tube through nose or mouth into stomach; used for short term <6 weeks; easily inserted; risk for aspiration pneumonia; potential discomfort; remains in place between meals; can be administered intermittent or continuous. Short term enteral feeding; may allow feeding after gastric surgery; difficult to place and maintain. Used for long term tube feedings into stomach of patients; often used for alterations in swallowing; less discomfort than nasogastric, can be inserted at bedside with local anesthesia; risk of skin breakdown around tube; contraindicated in peritonitis, ascites, morbid obesity, obstruction, esophageal obstruction or reflux. Formula can be given at night as intermittent, continuous, or cyclic. Direct access to jejunum when stomach must be bypassed; potential for dumping syndrome/diarrhea; lower risk of aspiration; pumped with slow infusion working up to strength/volume needed to meet nutritional needs of the patient. Always increase rate first, then strength.

Rombeau J, Caldwell M: Clinical Nutrition: Enteral and Tube Feeding, W.B. Saunders, 1990 SpringNet, CE Connection, Internet

9-12

TUBE FEEDING FORMULAS Type Isotonic balanced

Examples (partial list) Osmolite, Isocal

Complete balanced HC complete

Ensure, Nutren 1.0, Resource, Sustacal, Boost Ensure Plus, Comply, Isosource, Nutren 1.5, Boost Plus Ensure HN, Magnacal, TwoCal HN, Nutren 2, Impact, Respalor Ensure Fiber,Ultracal, Jevity, Sustacal Fiber, Compleat Mod. Vital HN, CriticareHN, TraumaCal, Peptamen Propeptite, Vivonex + Glucerna, Choice DM

High nitrogen

Fiber containing

Partially hydrolyzed elemental Glucose intolerance Specialized for CKD

CKD: Suplena, Amin-Aid On Dialysis: Nepro, MagnaCal Renal, NutriRenal

Characteristics Osmolality between 280-350 mOsm/kg water; 1 kcal/ml Osmolality more than 350 mOsm/kg water; 1 kcal/ml Osmolality more than 350 mOsm/kg water; 1.5 kcal/ml

Indications Tube feeding is sole source of nutrition; calorie needs 2-3000/d Can be used to supplement normal diet or tube for 2-3000 kcal/d Oral supplement or tube for reduced volume and high calories

Can be isotonic or hypertonic; 1-2 kcal/ml, more pro

Oral supplement or tube for higher protein w/ or w/ out higher kcals

Can be iso- or hypertonic; 1 kcal/mL; varied fiber

Primarily long term tube feeding to maintain normal bowel patterns

High pro level, hydrolyzed to peptides/aa, 1 kcal/ml Osmolality >350 mOsm/kg water Low CHO/minimize affect on blood sugar 1 kcal/mL Protein/electrolyte content modified for renal disease; 2 kcal/ml

Used with malabsorption/radiation treatment, usually administered by tube, but can be taken orally Type I or Type II diabetes or stressinduced hyperglycemia Oral or tube for patients unable to meet nutrition needs with traditional foods

Reference: SpringNet CE Connection, Internet

9-13

COMMON TUBE FEEDING PRODUCTS/1000 ml (Incomplete List) Kcal

CHO

PRO

Fat

Na+

K+

P

Ca++

Comply

1500

180

60

61

1200

1850

1200

1200

Criticare HN

1060

220

38

5.3

630

1310

530

530

Isocal

1060

135

34

44

530

1320

530

630

Isocal HN

1060

124

44

45

930

1610

850

850

Jevity

1060

154.7

44.3

34.7

930

1570

760

910

Nutren 1.0

1000

127

40

38

876

1248

668

668

Osmolite

1060

151.1

37.1

34.7

640

1020

535

535

Osmolite HN

1060

143.9

44.3

34.7

930

1570

760

760

Two-cal HN

2000

216

83.5

89.1

1460

2450

1055

1055

UltraCal HN+

1200

156

54

40

1350

1850

1000

1000

Product

References: Internet, Manufacturers’ Information

9-14

INTRADIALYTIC PARENTERAL NUTRITION (IDPN) Indications for Use

Potential Complications

All less intense therapies fail Permanent, significant GI impairment MD prescription Severe protein/calorie depletion Significant weight loss ADVANTAGES: Enhanced use of dialysis time Increased patient morale Convenient access to circulation Reduced catabolic stress Can replace dialysis aa losses Extra fluid is removed as solution is infused Less costly than TPN/hospitalization for complications of malnutrition May be tolerated best if infused over at least a 3 hour treatment

Loss of infused nutrients to dialysate

Possible Solutions

Damage to vascular access

Most retained with aa/glucose combination, add vitamins last 10 minutes Diluted 50-60 x before reaching endothelial wall

Hypoglycemia

Provide snack 30 min prior to end of infusion

Hyperglycemia

Can add insulin (BS >275 mg/dL) Decrease dextrose, slow infusion, adjust carbohydrate to patient body size Change dialysate/IDPN, oral supplements Decrease aa, provide adequate dialysis Encourage fluid compliance, decr volume, ensure adequate treatment time Increase Na+ intake, add Na+ to IDPN if MD order, increase total concentration, encourage fluid compliance, keep Hct at adequate level May be imbalance of aa/decrease lipid if due to fat/glycogen in liver Decrease aa if oral protein intake is high Infuse/increase lipids slowly, decrease concentration, d/c lipids if allergic reaction occurs

Electrolyte imbalance Azotemia Fluid overload Hypotension/Cramping/Hyponatremia

Elevated liver enzymes Acidosis Hyperlipidemia

K/DOQI: “Additional research is needed to document the absolute benefit of IDPN.” Reference: Satellite Healthcare Policy/Procedure Manual/Information from FMC Nutrition Support Service 9-15

GASTROINTESTINAL MOTILITY STUDIES Test Scintigraphic Study

Radiographic Pellet Study

Manometric Study

Description Solid phase emptying study determines stomach to jejunum* transit time. Injection or ingestion of radioisotope, usually mixed w/food followed by sequential gamma imaging of the abdomen. Ingestion of radiopaque pellets (or barium) followed by sequential abdominal radiographs to determine pellet transit time from stomach to jejunum.* Pressure measuring device passed into GI tract to take sequential pressure measurements to determine gastric emptying time.

Identifies Gastroparesis Small Bowel Dysmotility

Significant Findings < 3 hr transit time from stomach to jejunum or right colon does not qualify for parenteral nutrition.

Gastroparesis Small Bowel Dysmotility

3-6 hour transit time requires tube feeding trial, as does diagnosis of gastroparesis.

Gastroparesis

*If transit time to jejunum is >6 hours, use transit time to right colon. Reference: Medicare Parenteral Nutrition Policy, 1996 Other significant medical diagnoses to look for in the patient’s medical history: Amyloidosis, AIDS/ARC with related symptoms, chronic recurring pancreatitis, collagen vascular disease or myopathies, familial autonomic dystrophies, intestinal neuropathies, ischemic bowel disease, mesenteric infarction, myotonic or muscular dystrophy, motility disorders such as blind loop/dumping syndrome, delayed gastric emptying, gastric stasis, pyloric stenosis or obstruction, gastric outlet obstruction, gastroparesis. 9-16

IDPN SOLUTIONS Characteristic Lipid free Increased kcal, higher protein with lipids High protein, lipid free High protein, lipid free, limited vol High protein, high calorie (Use D70 to limit volume)

Prescription 250 cc D50 250 cc 10% aa 250 ml D50 550 ml 10% aa 250 ml 20% lipid 500 ml D50 550 ml 10% aa 250 ml D50 550 ml 10% aa 250 ml D70 500 cc 15% aa 250 ml 20% lipid

Total Volume 500 cc 1050 cc

1050 cc 800 cc 1000 cc

Formula Composition 125 gm dextrose 25 gm protein 125 gm dextrose 55 gm protein 50 gm fat 250 gm dextrose 55gm protein 125 gm dextrose 55 gm protein 175 gm dextrose 75 gm protein 50 gm fat

Kcals 525 1145

1070 645 1395

Reference: Goldstein, J. Intradialytic parenteral nutrition: Evolution and current concepts. J Ren Nutr, 1:9, 1991. Editorial Note: Many renal patients tolerate IDPN formulas that contain dextrose levels well above (2-3x) the published glucose oxidation rate of 5-8 mg/kg/minute. Rather than rely upon standard formulas, it may be prudent to formulate IDPN solutions based on individual patient needs and safe, effective utilization rates for specific substrates by starting slowly and working up to a level that provides maximum nutrients without adverse side effects (D70 is commonly used for decreased volume), base aa content on recommended protein levels (15% solutions are commonly used), and infuse 20% lipids at 1cc/min (FDA limits). Recent research (Satellite Dialysis Centers, Inc., Redwood City, CA) indicates that administration of IDPN with a high level of aa may increase urea generation. More research is needed to ascertain optimum therapy, appropriate solutions, nutrient levels, and document effectiveness. 9-17

RECOMMENDED TPN SOLUTION FOR ACUTE OR CKD Nutrient Amount Comment Mixed Amino Acids 1-1.5 gm/kg BW Base on treatment/GFR/stress/metabolic state, maint N2 bal kcals: Hypertonic Include dialysate kcals in CRRT, prevent CHO overfeeding 35-40 kcal/kg BW Dextrose 20- 30% total kcal Lipids (20%) Final concentration of electrolytes should include those in aa 35-40 mmol/L Electrolytes: Acetate solutions, adjust electrolyte content based on serum levels 25-35 mmol/L Chloride 5 mmol/day Calcium 2 mg /day Iron Monitor closely for refeeding syndrome in severely 4 mmol/day Magnesium malnourished patients; refeeding syndrome is characterized 8 mmol/day Phosphorus by acute changes in phosphorus, potassium, magnesium, ≤35 mmol/day Potassium vitamins, and/or glucose tolerance 40-50 mmol/L Sodium 60-100 mg Vitamin: Ascorbic Acid 200 µg\day Biotin 3 µg/day (IV/oral) B12 1 mg/day (IV/oral) Folic Acid 20 mg Niacin 10 mg Pantothenic Acid 10 mg Pyridoxine May need increased Vit K with lipid administration 2 mg of each Riboflavin, Thiamine 7.5 mg /wk (IV/oral) Vitamin K 10 IU/day Vitamin E Individualize Vitamin D Add if > 3 wk TPN Vitamin A/Trace Mins References: Monson P, et al: Nutrition in acute renal failure: A reappraisal for the 1990s. J Ren Nutr 4(2):58-77, 1994 Grant JP: Handbook of Total Parenteral Nutrition, W.B. Saunders, Philadelphia, 1992 Kopple JD, Massry S, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997 9-18

NUTRIENT CALCULATIONS FOR PARENTERAL NUTRITION 1. 2. 3. 4.

5.

6. 7. 8.

9.

Determine total daily calorie needs Determine protein needs Determine fluid allowance Determine the kcals to be provided by fat (usually 30-40% of total calories) Estimated kcals x desired percentage of fat = kcal as fat Example: 1700 kcals x 30% fat = 510 kcals from fat Convert to volume of lipid emulsion: 510 kcals /1.1 kcals/mL (10% emulsion) = 463 mL or 510 kcals/2.0 kcals/mL (20% emulsion) = 255 ml Determine kcals to be provided by protein: Estimated protein needs x kcals/gm protein Example: 70 gm protein x 4 kcals = 280 kcals as protein To calculate kcal:nitrogen ratio = Total kcals/grams of nitrogen. Calculate total kcals, determine grams of protein and divide by 6.25 to calculate grams of nitrogen. In this example, Kcal:N ratio = 1700/(70/6.25) or 152 kcal:1 gm nitrogen Determine the kcals to be provided by carbohydrate: Estimated kcal needs - (fat kcals + protein kcals) = kcals as carbohydrate Example: 1700 kcals - (510+280) = 910 kcals Common solutions are 70% dextrose, 10 or 15% aa, and 20% lipids. Determine volume of D70, 10% aa, and 20% lipid needed to reach target concentrations. Carbohydrate: 268 gm /70/100 mL = 383 mL 70% dextrose solution Protein: 70 gm/10/100mL = 700 mL 10% aa solution Fat: see step 2 above

Reference: Fish J: Worksheet for Calculation TPN. ADA Support Line XVII(6):10, 1995 Specialty Cards-Nutrition, 1998 9-19

NUTRITION SUPPORT MONITORING GUIDELINES IN THE STABLE DIALYSIS PATIENT Metabolic

TPN

IDPN

IPN

Tube Feeding

Albumin, Total protein 2-3 x/wk Monthly Monthly Monthly Blood gases, pH Weekly w/ problems w/ problems w/ problems BUN/Electrolytes Daily Stable, Monthly Monthly Monthly Ca++/P/ Mg++ 2-3x/wk Stable, Monthly Monthly Monthly Fluids Daily Daily Daily Daily Glucose Daily Pre/post tx Diab: Per exch As situation dictates Lipids 2-3 x/wk after test Monthly after test Monthly Monthly Liver enzymes Weekly Monthly Monthly Monthly UNA 2-3 x/wk NA NA NA ANTHROPOMETRICS Weight Daily Per treatment Daily Daily Arm anthropometrics/BMI Monthly Monthly Monthly Monthly NUTRITION Appetite NA Weekly Weekly Weekly nPNA w/UNA Monthly Quarterly Monthly Diet record NA Monthly Monthly Monthly DIALYSIS ADEQUACY Kt/V Monthly Monthly Quarterly Monthly/Quarterly Creatinine Clearance NA NA Quarterly Monthly/Quarterly Note: An individual monitoring schedule should be established for the medically unstable dialysis patient. The changing clinical situation will dictate the timing, aggressiveness, and extent of monitoring that should be undertaken. Patients who are receiving a combination of nutritional support should be monitored closely for refeeding syndrome. References: Goldstein DJ: IDPN: Evolution and current concepts, J Ren Nutr 1(1):9-22, 1991 Mitch WE, Klahr S, Eds: Nutrition and the Kidney. Lippencott-Raven, 1998 Nutrition Support Dietetics Core Curriculum, ASPEN, Second Edition, 1993

9-20

INTRAPERITONEAL AMINO ACIDS AS NUTRITION SUPPORT IN PD The cost of compounded aa/dextrose dialysate is not covered by Medicare. Some private insurance companies will pay for therapy on a case by case basis. The patient must meet criteria similar to those for IDPN. Solutions using amino acids as the osmotic agent are currently under consideration for FDA approval in the US. These bulk-produced, shelf-stable solutions (Nutrineal® Baxter Healthcare) are available in Canada, Europe, and Asia. Solutions Special Considerations Potential Benefits Side Effects Compounded Solutions Follow provider’s directions, but -Replace dialysate losses of Uremic symptoms (Generally 0.5-2% aa, with must be refrigerated and not overaa/protein. (Incr dialysis dose or decr aa) or without dextrose) heated. Usually suggest using at long dwell time for maximum -Promote anabolism absorption. Nutrineal® 1.1% aa solution, no glucose; 15 different aa incl 64% essential aa; 1 exch=22 gm aa; UF equivalent to a 1.5% dextrose, may require other hypertonic for fluid balance; 4-6 hour dwell allows 65-90% aa absorption depends on membrane transport characteristics

Dose: 1– 2 liter exchange/day w/in 1 hr before or after highest kcal meal. In extreme malnutrition can consider 2 exchanges/day with strict monitoring for acidosis, uremic symptoms, and fluid balance; alternate with glucose 2 year shelf-life; should be stored in original shipping carton until useprotected from sunlight; not microwaved Reduced glucose load may require an adjustment in insulin therapy.

-Improve nitrogen balance/ plasma aa patterns/serum proteins -Reverse/halt malnutrition progression; replace losses in peritonitis -Improve immune function -Boost energy -Improve patient’s sense of well-being -Improve appetite

Metabolic acidosis (decr aa/ incr alkalizing agent) N & V, other GI symptoms (decrease aa or identify and treat other causes)

Reference: Satellite Dialysis Centers, Redwood City, CA and Baxter Healthcare Asia, Nutrineal® Prescriber’s Guide 9-21

Clinical Associations with Negative Nitrogen Balance Loss of body weight/Diminished muscle mass Hypoproteinemic edema Impaired immunocompetence (humoral/cellular) Increased susceptibility to infection Poor wound healing Increased morbidity and mortality Reference: Dickerson WT: Nutrition in Clinical Management of Disease, Edward Arnold, 1988

Estimation of Nitrogen Balance Nitrogen balance = Nitrogen in - Nitrogen out Nitrogen in = Enteral + parenteral protein in grams 6.25 (converts protein to nitrogen) 1

Nitrogen out=Urinary urea nitrogen (UUN g/d) + insensible loss (0.5 gm N/day) + dialysate losses 1

HD est=1-1.5 g N/dialysis PD est=0.05-0.08 g aa/exch and 0.1+/-0.08 g Pro/hour of treatment (can double with peritonitis). CRRT est=1.5-2.0 g N/day

Reference: Monson P: Nutrition in acute renal failure: A reappraisal for the 1990s. J Ren Nutr 4(2):58-77, 1994 9-22