Acute Kidney Injury
Core concepts
Frame AKI by prerenal, intrinsic (tubular, glomerular, interstitial, vascular), and postrenal causes. Use the KDIGO definition (creatinine rise ≥0.3 mg/dL in 48 h or ≥1.5× baseline in 7 days; urine output <0.5 mL/kg/h for 6 h).
Prerenal: BUN/Cr >20, FENa <1% (except on diuretics), bland urine, responds to volume. **ATN:** muddy brown casts, FENa >2%, prolonged insult. Postrenal: bladder scan, obstruction-relieve promptly. Contrast-associated AKI and pigment nephropathy (rhabdomyolysis, hemolysis) are high-yield. Hepatorenal syndrome requires cirrhosis with ascites, exclusion of other causes, no response to albumin challenge, and absence of shock.
Traps
FENa is unreliable with diuretics, CKD, or contrast; FEUrea helps. Creatinine lags injury-use urine output and context. Urine sodium can be low in early obstruction or contrast. Don't miss abdominal compartment syndrome or cast nephropathy (myeloma) in unexplained AKI. Rhabdomyolysis: check CK, treat with aggressive fluids, watch for hyperkalemia and hypocalcemia.
Rule of thumb
If the patient improves with a fluid challenge and has a bland sediment, prerenal is likely; if casts and no response, intrinsic disease-then look for nephrotoxins, ischemia, or obstruction.
Worked example
A trauma patient with dark urine, CK 40,000, K 6.2, and rising creatinine: diagnosis pigment nephropathy/rhabdomyolysis; treat with isotonic fluids, monitor electrolytes, and consider dialysis for refractory hyperkalemia.