Os214 20060306 Grp10a Chronic Renal Failure

CHRONIC RENAL FAILURE

OS 214 EXCRETORY

GROUP

dR. IRMINGARDA GUECO, MARCH 6, 2005

OUTLINE Discuss the pathophysiology of CRF/ESRD. Distinguish the pathophysiology of CRF from ESRD. Describe the clinical manifestations of CRF/ESRD. Correlate clinical history and physical examination findings with the pathophysiology of CRF/ESRD. 5. Discuss the laboratory findings in CRF/ESRD. 6. Discuss the supportive management of patients with CRF/ESRD. 7. Explain the principles and indications of renal replacement therapies, including renal transplantation. 8. Construct an algorithm on the approach to a patient with CRF/ESRD. We would like to acknowledge the KREMLINS for the soft copy of this trans  Notes taken during the lecture are in arial size 8 1. 2. 3. 4.

Why separate acute from chronic renal failure? - Management is different - Manifestations may be similar - Prognosis is different: Chronic Renal Failure – irreversible; Acute Renal Failure – reversible Functions of the Kidney Excretory function Maintenance of Acid – Base Balance Maintenance of Fluid and Electrolyte Balance Maintenance of Ca-Phosphate Balance (Mineral balance)

Vitamin D production Erythropoeitin Production

Measured using: BUN, creatinine pH, HCO3, pCO2 Osmolality, water, Na, K, Cl Ca, Phosphates (Mg) Calcium Hgb, hct for confirmation

Chronic Renal Failure (CRF) -Pathophysiologic process which is a result of varied conditions that leads to irreversible destruction of nephrons, ultimately leading to End Stage Kidney Disease (ESRD). -Sum of all processes that happen cause by various diseases such as DM, hpn, GN, lupus, secondary causes due to multiple myeloma, etc. - Slow deterioration of kidney function - Loss of nephrons  other nephrons try to compensate during CRF phase, you don’t see manifestations of ESRD - Normal GFR men:100ml/min; women:85ml/min - Just keep in mind that the key word in CRF is COMPENSATION - DO NOT MAKE THE MISTAKE OF DIALYSING A PATIENT WITH CRF! Spectrum of CRF: Normal kidney

CRF (>3mos)

ESRD

Pathophysiology -Long term reduction of renal mass / function which initially leads to compensatory hypertrophy and function. Eventually this leads to sclerosis of the remaining nephron, resulting to ESRD. Stages of Chronic Renal Disease Stage

Description

1

At increased risk of kidney damage with normal or increased GFR Kidney damage with mildly decreased GFR Moderately decreased GFR Severely decreased GFR

2 3 4

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GFR, mL/min per 1.73 m2 90 (with CRD risk factors) 90 60-89 30-59 15-29

5

Renal Failure (ESRD)

< 15

GFR • CRF: 16-89 mL/min • ESRD: <15 mL/min Difference between CRF & ESRD in terms of Pathophysiology CRF – there is hyperfiltration, some amount of compensation ESRD – no more compensation; all other organ systems will end up with some kind of dysfunction Kidney Function Excretory Function

Maintenance of AcidBase Balance Maintenance of Fluid & Electrolyte Balance

Maintenance of CalciumPhosphate Balance Vitamin D Production

Erythropoietin Production

Chronic Renal Failure (CRF) No signs / symptoms ↑ BUN ↑ Creatinine, ↑ Cystatin C No Manifestations Normal acidbase balance ↑ BP NVE Crackles Edema Na – Normal K – Normal or ↑ No manifestations ↑ Phosphate ↓ Ca No manifestations ↓ Calcitriol (see diagram below) Weakness Dizziness Pallor Easy Fatigability ↓ Hemoglobin

End-Stage Renal Disease (ESRD) Nausea / vomiting ↑↑ BUN ↑↑ Creatinine, ↑↑ Cystatin C ↑ RR – Kussmaul breathing Metabolic Acidosis ↑ RR Arrythmia NVE Crackles Edema Na – Normal K–↑ Osteitis fibrosa cystica ↑↑ Phosphate ↓↓ Ca Osteomalacia ↓ Calcitriol

Weakness Dizziness Pallor Easy Fatigability ↓↓ Hemoglobin

Excretory function: • ≤1.5mg creatinine • 10-20 BUN depending on level of hydration • Cystatin- only used in lab research for now Maintenance of Acid-Base Balance: • Still with compensation Maintenance of Fluid & Electrolyte Balance: • For fluids, think also of sodium going along with it • Creatinine clearance >60, accumulation of Na • Increased BP: CM, lupus, GN • No signs/symptoms, normal BP: may also have renal failure, creatinine worsening • Buko juice: causes hyperkalemia; so AVOID DRINKING BUKO JUICE WHEN YOU HAVE KIDNEY PROBLEMS UNLESS YOU HAVE LOW POTASSIUM • Buko juice, bananas  good fore people with diarrhea • Nephrologists should therefore identify patients are Na or K wasters. If this is the case then don’t let them avoid Na of K. Maintenance of Calcium-Phosphate Balance • >25% creatinine clearance is still normal Vitamin D Production • Calcitriol- only in lab research for now • (Please refer to table at last page) Why is there an increase in phosphates in ESRD?  because the poorly functioning kidney

OS 214 GROUP

CHRONIC RENAL FAILURE

EXCRETORY

can’t eliminate them all. The phosphate binds with calcium  leading to a decrease in ionized calcium  leading to secondary hypoparathyroidism Erythropoietin Production • In DM, anemia occurs early

Management of Chronic Renal Failure A. Comprehensive strategy for renoprotection in patients with chronic renal disease Intervention Therapeutic Goal Specific renoprotective therapy Proteinuria <0.5 g/day ACE inhibitor or ARB GFR decline <2 treatment ml/min/year Adjunctive cardiorenal protective therapy Additional <130/80 mm Hg antihypertensive therapy Dietary protein restriction Dietary salt restriction 0.6-0.8 g/kg/day Tight glycemic control 3-5 g/day in diabetes Reduce elevated AIC < 6.05 % calcium-phosporous Normal values Lipid lowering therapy Anti-platelet therapy Consider correction of anemia Smoking cessation Weight control • • • •

LDC-C <100mg/dl Thrombosis prophylaxis Hb > 12g/dl Abstinence Ideal body weight

Level of proteinuria determines the level of dietary protein restriction in patients Reduce elevated electolyte Ca and P if <25%, it merits checking The lecturer considers correction of anemia if Hb 11-12g/dl Lipid lowering therapy (Statins)

B. Avoid insults to the kidney

•Volume depletion- diarrhea •Nephrotoxins- aminoglycosides, radiocontrast material •NSAID- COX2 inhibitors, mefenamic acid, naproxene, indomethacin

C. Preparation for ESRD management • Psychological • Renal Replacement Therapy, options o Dialysis – Vascular Access o Transplant – Recipient Donor Work-Up * with a creatinine clearance of 20 or 25, you can start discussing dialysis with the patient End Stage Renal Disease Please see table on first page Excretory function:  Nausea and vomiting- SSX of accumulation of BUN, creatinine Maintenance of Acid-Base Balance: • metabolic acidosis Maintenance of Fluid & Electrolyte Balance: • body can’t eliminate waste products because it can’t compensate; arrhythmia due to increased K Maintenance of Calcium-Phosphate Balance • Phosphate retained, binds to Ca, absence of Vit D3 decreased gut absorption of Ca Vitamin D Production Erythropoietin Production

•Anemia insidious in onset  so you may have SSX in ESRD

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dR. IRMINGARDA GUECO, MARCH 6, 2005

Pathophysiology: fibrosis – no more compensation in whatever aspect of excretion Management of ESRD A. Supportive 1. Nutrition 2. Psychological 3. Control BP 4. Maintain Hb at 110-120 g/dl with erythropoietin oral iron is not absorbed very\well by uremic patient; it’s better to give it to them IV

5. Fluid and electrolyte balance 6. Acid-base homesotasis 7. Maintain Ca and Phosphate balance –

give Calcium carbonate or Calcium acetate with meals. You eat meat, and meat has phosphate. Para habang nakakapagbigay ka ng calcium, nakakapag prevent ka na rin ng absorption ng phosphate. You “shoot two birds with one stone”

B. Renal Replacement Therapy 1. Dialysis 2. Hemodialysis 3. Peritoneal Dialysis 4. Transplant 5. - Consider dialysis if creatinine clearance is about 20ml/min - Uremic symptoms present with nausea and vomiting. If the disease is not ESRD, consider other etiologies for the said symptoms - Excess fluid in the body – volume overload – diuretics won’t help coz kidneys are already sclerosed

Renal Replacement Therapy in CRF - indicated when metabolic abnormalities can no longer be controlled with conservative management or when signs and symptoms of uremia developed - No absolute value in terms of CR by which you will start your RRT Indications for Dialysis - volume overload - intractable metabolic acidosis - hyperkalemia - uremic state (encephalopathy, pericarditis) - azotemia without uremic manifestations CASE A 24-year old male diagnosed with chronic glomerulonephritis was admitted for nausea and vomiting. Maintenance of ACE inhibitors with HCTZ (Hydrochlorothiazide) was given. His last follow-up a week ago showed a Cr 1.8 mg%. Three days PTA he had copious diarrhea and was unable to take anything including medicines. He noted decreased urine output. He felt weak and later developed nausea and vomiting. PE: BP = 90/60 PR = 110/min RR = 25/min Sunken eyeballs, dry skin and mucous membranes BUN 80mg/dL; Cr 10mg/dL; K 6meq/L; Na 132 meq/L ABG: pH 7.2; HCO3 11meq/L; CO2 20meq/L Hgb: 15gm/dl (N14-17) Hematocrit: 45 (hemoconcentrated) Urinalysis: Sp gr = 1.010, (4+) protein, (–) sugar 4-5 RBCs/hpf, 10-15 WBCs/hpf What is your diagnosis? a. Acute renal failure b. Chronic renal failure c. End stage renal failure d. Acute on chronic renal failure

CHRONIC RENAL FAILURE

OS 214 EXCRETORY

GROUP

dR. IRMINGARDA GUECO, MARCH 6, 2005

Answer: Acute on Chronic Renal Failure

Answer: Dialysis

What finding tells us that the patient has renal failure? a. K b. pH c. creatinine d. urinalysis –just a reflection that something’s wrong, but

If anemic (Hb 10g/dl), what is the mgt?

not specific for renal failure

Answer: Creatinine What is the cause of the ABG finding? e. Chronic GN f. Diarrhea g. Vomiting h. Acute renal failure

Answer: Give erythropoietin. If <10 g/dl, transfusion From block B:  Hyperkalemia – don’t give diuretics because patient is dehydrated; give sodium bicarbonate -> push K inside the cell, decrease K levels contraindication of sodium bicarbonate: presence of NVE, crackles, edema  Hydration removes hemoconcentration. After hydration, observe true level of Hgb. If low Hgb -> address anemia.  If Pt does not improve -> Ultrasound, check for other renal problems

Answer: Diarrhea and ARF (acidosis) How should you manage this patient? a. kidney transplant b. dialysis c. supportive management d. observe Answer: Supportive Management Management:  Hydrate patient  For increased K, give sodium bicarbonate- shoot two birds with one stone  not only do you decrease K you also replace the lost HCO3  Treat the cause of diarrhea  Nutrition: don’t focus on it yet. Just follow treatment for diarrhea  Follow up BUN, creatinine. If it improves, don’t do anything. Take note that there’s a 3-4 day period before creatinine drops. Hypovolemia: low BP, sunken eyeballs, dry skin, mucous membrane Increased RR implies metabolic acidosis Hemoconcentration due to diarrhea

If the creatinine changed from 1.8 to 9mg, but the patient has nausea and vomiting, Bp=130/80, no diarrhea, eyeballs not sunken, (+)edema, what is the management?

Decreased Renal Function

Decreased 1.25 (OH)2D3

Hyperphosphatemia

Decreased expression of calciumsensing receptor

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AI3+ Intoxication

Accumulation of ß2 microglobulin

Decreased ionized Ca2+

Hyperparathyroidism

Hyperplasia of the parathyroid glands

Osteitis fribrosa cystica (high-turnover bone disease)

Metabolic acidosis

Osteomalacia

Adynamic bone disease

Dialysis-related amyloidosis

Excess Ca and vit D, PD, diabetes