Renal System

AKI is a rise in serum creatinine of ≥0.3 mg/dL within 48 hours, a rise to ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/h for ≥6 hours. It is categorized as prerenal, intrinsic, or postrenal.

Prerenal (hypoperfusion: hypovolemia, heart failure, sepsis), intrinsic/renal (ATN, AIN, glomerular, vascular), and postrenal (obstruction: BPH, stones, tumor). Identifying the category drives workup and management.

Prerenal: BUN:creatinine ratio >20:1, FENa <1%, urine Na <20 mEq/L, high urine osmolality (>500), bland sediment. ATN: BUN:Cr ~10–15:1, FENa >2%, urine Na >40, isosthenuric (~300), muddy-brown granular casts.

FENa = (urine Na × plasma Cr) / (plasma Na × urine Cr) × 100. <1% = prerenal (intact tubular Na avidity); >2% = ATN. FENa is unreliable if the patient is on diuretics—use FEUrea (<35% = prerenal) instead.

Muddy-brown granular casts (and renal tubular epithelial cell casts). ATN is most often caused by prolonged ischemia or nephrotoxins (aminoglycosides, contrast, myoglobin from rhabdomyolysis).

Fever, rash, and eosinophilia—often after a culprit drug (NSAIDs, beta-lactams, PPIs, sulfa). Urinalysis shows WBCs and white-cell casts; urine eosinophils may be present. Treatment is stopping the offending drug ± corticosteroids.