Renal · Chronic Kidney Disease
The facts most likely to be tested
Diabetes mellitus is the leading cause of end-stage renal disease (ESRD) in the United States, followed by hypertension.
Renal osteodystrophy in ESRD is characterized by secondary hyperparathyroidism due to hyperphosphatemia, hypocalcemia, and decreased 1,25-dihydroxyvitamin D production.
Uremic pericarditis is a life-threatening complication of ESRD that requires urgent hemodialysis to prevent cardiac tamponade.
Anemia of chronic kidney disease is primarily caused by erythropoietin deficiency and is treated with erythropoiesis-stimulating agents (ESAs) after correcting iron deficiency.
Platelet dysfunction in uremia leads to a prolonged bleeding time despite a normal platelet count, which is best treated with desmopressin (DDAVP) if active bleeding occurs.
Hyperkalemia is the most dangerous electrolyte abnormality in ESRD, presenting with peaked T waves on ECG and requiring immediate stabilization with intravenous calcium gluconate.
Renal replacement therapy via hemodialysis is indicated for patients with refractory hyperkalemia, volume overload, uremic encephalopathy, or pericarditis.
Vignette unlocked
A 62-year-old male with a history of type 2 diabetes and hypertension presents to the emergency department with fatigue, nausea, and pruritus. Physical examination reveals a pericardial friction rub and bilateral pitting edema. Laboratory studies show a BUN of 110 mg/dL, creatinine of 8.5 mg/dL, potassium of 6.2 mEq/L, and hemoglobin of 8.2 g/dL. An ECG demonstrates peaked T waves.
What is the most appropriate next step in management?
Urgent hemodialysis
The patient exhibits signs of uremic pericarditis and severe electrolyte derangement (hyperkalemia), which are absolute indications for urgent renal replacement therapy.
Full handout
High yield triage
Etiology / Epidemiology
Diabetes mellitus is the leading cause; hypertension is the second. ESRD is defined as GFR <15 mL/min/1.73m².
Clinical Manifestations
Look for uremic frost, pericardial friction rub, and anemia of chronic disease. Uremic encephalopathy is a medical emergency.
Diagnosis
GFR <15 mL/min/1.73m² for >3 months or requirement for renal replacement therapy.
Treatment
Kidney transplantation is the gold standard. Hemodialysis is the primary bridge therapy.
Prognosis
High cardiovascular mortality. Monitor Kt/V urea to ensure adequate dialysis clearance.
Full handout
Epidemiology & Etiology
ESRD represents the final stage of chronic kidney disease. Diabetes mellitus accounts for nearly 45% of cases, followed by hypertension and glomerulonephritis. Prevalence is highest in African American and Native American populations.
Pertinent Anatomy
The nephron unit is progressively destroyed, leading to loss of glomerular filtration and tubular function. Vascular access for dialysis requires a native arteriovenous fistula or synthetic graft.
Pathophysiology
Irreversible nephron loss triggers compensatory hyperfiltration in remaining units, accelerating sclerosis. Failure of endocrine function leads to decreased erythropoietin production and secondary hyperparathyroidism. Uremic toxins accumulate, causing systemic multi-organ dysfunction.
Clinical Manifestations
Patients present with uremic frost (white urea crystals on skin), pericardial friction rub (sign of uremic pericarditis), and asterixis. Uremic encephalopathy manifests as confusion or seizures. Chronic findings include anemia, pruritus, and bone pain from renal osteodystrophy.
Diagnosis
Diagnosis is based on a GFR <15 mL/min/1.73m² sustained for >3 months. Renal ultrasound is the gold standard for assessing kidney size; small, echogenic kidneys suggest chronicity. Labs show hyperkalemia, hyperphosphatemia, and hypocalcemia.
Treatment
Kidney transplantation offers the best survival and quality of life. Hemodialysis is initiated for pericarditis, refractory hyperkalemia, or fluid overload. Avoid magnesium-containing antacids and adjust all renally cleared medications.
Prognosis
Cardiovascular disease is the leading cause of death. Patients require strict monitoring of Kt/V urea and phosphorus levels to prevent metabolic bone disease. Long-term survival depends on vascular access patency and immunosuppression adherence.
Differential Diagnosis
Acute Kidney Injury: rapid rise in creatinine over hours/days
Nephrotic Syndrome: massive proteinuria >3.5g/day with hypoalbuminemia
Polycystic Kidney Disease: bilateral flank masses and family history
Multiple Myeloma: Bence-Jones proteinuria and lytic bone lesions
Renal Artery Stenosis: refractory hypertension with abdominal bruit