Progressive loss of kidney function over ≥3 months, defined by eGFR <60 mL/min/1.73 m² or signs of kidney damage (e.g., persistent albuminuria).
Very common (≈14% of adults) and a leading cause of end-stage renal disease requiring dialysis or transplant. Causes systemic issues (anemia, bone disease, acidosis, CV risk) and frequently appears on exams linking kidney function to widespread effects.
Often asymptomatic until late stages; early clues are subtle (nocturia, fatigue). Advanced CKD causes uremic symptoms (anorexia, pruritus, confusion), plus edema, hypertension, and anemia (due to low EPO).
Adult causes: diabetes (diabetic nephropathy) and hypertension are most common; also chronic glomerular diseases (e.g., IgA nephropathy), polycystic kidney disease, or long-standing obstruction (stones, BPH).
Pediatric causes: usually CAKUT (congenital anomalies of kidney & urinary tract like reflux or posterior urethral valves), reflux nephropathy from recurrent UTIs, hereditary nephropathies (e.g., nephronophthisis), or chronic glomerulopathies.
Confirm chronicity: check old creatinine trends and kidney size (small, shrunken kidneys suggest chronic disease).
Stage the CKD: GFR categories 1–5 (stage 3 starts at GFR <60, stage 5 is <15 or dialysis) and classify albuminuria (A1 <30, A2 30–300, A3 >300 mg/g).
Evaluate cause: get urinalysis (protein, hematuria, casts) and urine ACR (albumin-creatinine ratio) to quantify proteinuria; consider serologies for glomerulonephritis if indicated.
Imaging: perform renal ultrasound to assess size and rule out obstruction or structural abnormalities (CKD kidneys often appear small and scarred, except in diabetes or PKD which may be enlarged).
Monitor for complications: regularly check hemoglobin (for anemia of CKD), electrolytes (especially potassium), bicarbonate (metabolic acidosis), and calcium/phosphate/PTH (secondary hyperparathyroidism).
Condition
Distinguishing Feature
Prerenal azotemia
reversible ↓GFR from low perfusion (e.g., dehydration, heart failure)
Acute glomerulonephritis
active urinary sediment (RBC casts), shorter duration, often nephritic syndrome
Postrenal (obstructive) AKI
acute decline due to obstruction (hydronephrosis on imaging, resolves if blockage relieved)
Slow the progression: strict BP control (<130/80) with ACEi/ARB (especially if proteinuria); optimize glycemic control in diabetics; avoid nephrotoxins (NSAIDs, IV contrast).
Manage complications: erythropoietin-stimulating agents for anemia, phosphate binders and calcitriol for renal bone disease, bicarbonate supplements for metabolic acidosis, diuretics and salt restriction for volume overload, etc.
Plan for renal replacement: when GFR falls <20–30 (stage 4), educate and prepare for dialysis (vascular access for hemodialysis) or transplant evaluation; start dialysis for uremic symptoms or severe electrolyte imbalances.
Fewer nephrons → surviving nephrons hyperfilter to compensate, which over time causes fibrosis (hyperfiltration injury accelerates CKD).
CKD usually leads to small kidneys on imaging due to scarring (exceptions: diabetic nephropathy and PKD can have normal or large kidneys).
Signs of uremia (encephalopathy, pericarditis, asterixis, bleeding) or refractory hyperkalemia/fluid overload → urgent dialysis is indicated.
Sudden GFR decline in CKD patient—think acute on chronic (e.g., volume depletion, nephrotoxic drug, obstruction) which may be reversible if addressed promptly.
