Chronic Kidney Disease for USMLE Step 2

Chronic Kidney Disease (CKD) for the USMLE Step 2 Exam
Definition
  • Chronic Kidney Disease (CKD): Progressive, irreversible decline in kidney function lasting at least 3 months, marked by a reduction in glomerular filtration rate (GFR) or evidence of kidney damage (e.g., proteinuria, hematuria, or imaging abnormalities).
  • Diagnosis Criteria:
    • GFR <60 mL/min/1.73 m² for ≥3 months, or
    • Evidence of kidney damage (e.g., albuminuria ≥30 mg/g, abnormal urine sediment) for ≥3 months.
Staging (KDIGO)
  • Stage 1: GFR ≥90 mL/min/1.73 m² with evidence of kidney damage.
  • Stage 2: GFR 60–89 mL/min/1.73 m² with evidence of kidney damage.
  • Stage 3:
    • 3a: GFR 45–59 mL/min/1.73 m².
    • 3b: GFR 30–44 mL/min/1.73 m².
  • Stage 4: GFR 15–29 mL/min/1.73 m².
  • Stage 5: GFR <15 mL/min/1.73 m² (end-stage renal disease, ESRD).
Etiology
  • Diabetes Mellitus (DM): The leading cause of CKD due to chronic hyperglycemia, which causes glomerular hyperfiltration and nephron loss over time.
  • Hypertension: Chronic high blood pressure leads to nephrosclerosis and ischemic injury to the kidneys, progressively reducing renal function.
  • Glomerulonephritis: Inflammatory damage to the glomeruli, often due to autoimmune conditions like lupus or post-infectious causes.
  • Polycystic Kidney Disease (PKD): A genetic condition causing cyst formation in the kidneys, leading to progressive destruction of renal parenchyma.
  • Other Causes:
    • Chronic obstructive uropathy (e.g., from kidney stones or benign prostatic hyperplasia).
    • Long-term use of nephrotoxic drugs (e.g., NSAIDs, certain antibiotics).
Pathophysiology
  • Hyperfiltration Injury: Loss of nephrons leads to compensatory hyperfiltration in remaining nephrons, which further damages glomeruli and causes progressive nephron loss.
  • Glomerulosclerosis and Fibrosis: Chronic kidney damage results in glomerular scarring (glomerulosclerosis) and tubulointerstitial fibrosis, worsening renal function.
  • Uremia: Accumulation of waste products (uremic toxins) occurs as kidney function declines, leading to symptoms like fatigue, anorexia, pruritus, and confusion in advanced stages.
Clinical Presentation
  • Early Stages (1–3):
    • Usually asymptomatic, with proteinuria, hypertension, or edema as early signs.
    • Laboratory abnormalities such as elevated serum creatinine or albuminuria may be detected.
  • Late Stages (4–5):
    • Symptoms of uremia: Nausea, vomiting, pruritus, fatigue, cognitive dysfunction.
    • Hypertension: Common due to volume overload and increased RAAS activation.
    • Anemia: Resulting from reduced erythropoietin production.
    • Bone Disease: Due to secondary hyperparathyroidism and altered calcium-phosphorus metabolism.
    • Fluid Overload: Peripheral edema, dyspnea, and pulmonary edema.
Signs & Symptoms of Chronic Kidney Disease
Diagnosis
  • Laboratory Tests:
    • Serum Creatinine and GFR: Used to stage CKD.
    • Urinalysis: Detects proteinuria and hematuria; an albumin-to-creatinine ratio (UACR) is used to quantify proteinuria.
    • Electrolytes: Hyperkalemia, hyperphosphatemia, and metabolic acidosis are common in advanced CKD.
  • Imaging:
    • Renal Ultrasound: Useful for detecting small, atrophic kidneys in advanced disease or enlarged polycystic kidneys in PKD.
Management
  • Control of Underlying Causes:
    • Diabetes: Tight glycemic control with HbA1c <7% to slow disease progression.
    • Hypertension: Use of ACE inhibitors or ARBs to reduce proteinuria and slow progression, with a target BP <130/80 mmHg.
  • Dietary Management:
    • Protein Restriction: Reduces nitrogenous waste buildup (0.8 g/kg/day).
    • Sodium Restriction: To prevent fluid overload and hypertension.
    • Phosphorus Restriction: To manage hyperphosphatemia and prevent bone disease.
  • Management of Complications:
    • Anemia: Treated with erythropoiesis-stimulating agents (ESAs) and iron supplementation.
    • Hyperkalemia: Managed with dietary restriction, potassium binders, and loop diuretics.
    • Metabolic Acidosis: Sodium bicarbonate supplementation to maintain normal bicarbonate levels.
    • Bone Disease: Phosphate binders, vitamin D analogs, and calcimimetics to prevent renal osteodystrophy.
  • End-Stage Renal Disease (ESRD):
    • Dialysis: Indicated when patients develop uremic symptoms or severe complications like hyperkalemia, acidosis, or volume overload.
    • Kidney Transplantation: The best long-term treatment option for ESRD.
Complications
  • Cardiovascular Disease: Leading cause of death in CKD patients due to hypertension, dyslipidemia, and uremia.
  • Electrolyte Imbalances: Hyperkalemia and metabolic acidosis can lead to life-threatening complications.
  • Renal Osteodystrophy: Caused by disordered calcium-phosphate metabolism, leading to bone pain and increased fracture risk.
Key Points
  • CKD is diagnosed by reduced GFR (<60 mL/min/1.73 m²) or evidence of kidney damage (e.g., proteinuria) for ≥3 months.
  • Common causes include diabetes, hypertension, and glomerulonephritis.
  • Management focuses on controlling underlying causes, dietary modifications, and managing complications like anemia, hyperkalemia, and bone disease.
  • ESRD requires dialysis or kidney transplantation.
  • Cardiovascular disease is the leading cause of death in CKD patients, emphasizing the importance of early intervention.