Chronic Renal Failure

Chronic Renal Failure the First Affiliated Hospital of Zhengzhou University

BACKGROUND

chronic kidney disease (CKD)

K/DOQI defines : either kidney damage or a decreased kidney glomerular filtration rate (GFR) of <60 mL/min/1.73 m2 for 3 or more months.

classification of the stages of CKD Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2) Stage 2: Mild reduction in GFR (60-89 mL/min/1.73 m2) Stage 3: Moderate reduction in GFR (30-59 mL/min/1.73 m2) Stage 4: Severe reduction in GFR (15-29 mL/min/1.73 m2) Stage 5: Kidney failure (GFR <15 mL/min/1.73 m2 or dialysis)

PATHOPHYSIOLOGY

Approximately 1 million nephrons are present in each kidney, each contributing to the total GFR. the kidney has an innate ability to maintain GFR by hyperfiltration and compensatory hypertrophy of the remaining healthy nephrons. urea and creatinine start to show significant increases in plasma levels only after total GFR has decreased to 50% .

Factors cause progressive renal injury Systemic hypertension Acute insults from nephrotoxins or decreased perfusion Proteinuria Increased renal ammoniagenesis with interstitial injury Hyperlipidemia Hyperphosphatemia with calcium phosphate deposition Decreased levels of nitrous oxide

EPIDEMIOLOGY

In 1999, there were 340,000 such patients, by 2010, this number is projected to reach 651,000. Japan has the highest prevalence per million population, with the United States taking second place.

The 5-year survival rate for a patient undergoing chronic dialysis in the United States is approximately 35%. This is approximately 25% in patients with diabetes. The most common cause of death in the dialysis population is cardiovascular disease.

the incident rate for blacks is nearly 4 times that for whites. the incident rate of ESRD cases is higher for males with 409 per million population in 2002 compared to 276 for females. the highest incidence rate of ESRD occurs in patients older than 65 years.

CLINICAL

Hyperkalemia usually develops when GFR falls to less than 20-25 mL/min because of the decreased ability of the kidneys to excrete potassium. Metabolic acidosis often is mixed, non–anion gap and anion gap, In CKD, the kidneys are unable to produce enough ammonia in the proximal tubules to excrete the endogenous acid into the urine in the form of ammonium.

Extracellular volume expansion and total-body volume overload results from failure of sodium and free water excretion. Normochromic normocytic anemia principally develops from decreased renal synthesis of erythropoietin. Secondary hyperparathyroidism develops because of hypocalcemia, decreased renal synthesis of 1,25-dihydroxycholecalciferol (1,25-dihydroxyvitamin D, or calcitriol), and hyperphosphatemia.

Pericarditis - Can complicate with cardiac tamponade Encephalopathy - Can progress to coma and death Peripheral neuropathy Restless leg syndrome GI symptoms - Anorexia, nausea, vomiting, diarrhea Skin manifestations - Dry skin, pruritus, ecchymosis Fatigue, increased somnolence, failure to thrive Malnutrition Erectile dysfunction, decreased libido, amenorrhea Platelet dysfunction with tendency to bleeding

Causes Vascular disease Primary glomerular disease Secondary glomerular disease Tubulointerstitial disease Urinary tract obstruction

WORKUP

Lab Studies

Elevated serum urea and creatinine Hyperkalemia, low serum bicarbonate, hypocalcemia, hyperphosphatemia, hyponatremia Normochromic normocytic anemia Twenty-four–hour urine collection for total protein and CrCl

Imaging Studies Plain abdominal x-ray Intravenous pyelogram Renal ultrasound Renal radionuclide scan CT scan MRI

TREATMENT

Medical Care Delaying or halting progression of CKD Treatment of the underlying condition if possible Aggressive blood pressure control to target values Use of ACE inhibitors as tolerated Aggressive glycemic control Protein restriction Treatment of hyperlipidemia to target levels Avoidance of nephrotoxins

Treating pathologic manifestations of CKD

Anemia with erythropoietin Hyperphosphatemia with dietary phosphate binders and dietary phosphate restriction Hypocalcemia with calcium supplements +/- calcitriol Hyperparathyroidism with calcitriol or vitamin D analogs Volume overload with loop diuretics or ultrafiltration Metabolic acidosis with oral alkali supplementation Uremic manifestations with chronic renal replacement therapy Cardiovascular complications

Timely planning for chronic renal replacement therapy

Early education regarding natural disease progression Timely placement of permanent vascular access Timely elective peritoneal dialysis catheter insertion Timely referral for renal transplantation

Consultations Early nephrology referral Renal dietitian Vascular surgery for permanent vascular access General surgery for peritoneal catheter placement Referral to renal transplant center

Diet Protein restriction,but precaution Malnutrition Phosphate restriction starting early in CKD Potassium restriction Sodium and water restriction as needed to avoid volume overload