Clinical meaning
Acute kidney injury (AKI) is classified by etiology: prerenal (60-70%), intrinsic renal (25-30%), and postrenal (5-10%). Prerenal AKI results from reduced renal perfusion (hypovolemia, heart failure, sepsis) without structural kidney damage; autoregulatory mechanisms maintain GFR until mean arterial pressure falls below 65-70 mmHg, at which point afferent arteriolar dilation is maximal. Intrinsic AKI involves structural damage, most commonly acute tubular necrosis (ATN) from ischemia or nephrotoxins. Ischemic ATN causes proximal tubular cell necrosis, loss of brush border, sloughing of cells into tubular lumen (muddy brown granular casts), backleak of filtrate through damaged epithelium, and tubuloglomerular feedback causing afferent arteriolar constriction. Nephrotoxic ATN results from direct tubular cell toxicity (aminoglycosides, contrast dye, cisplatin, myoglobin). KDIGO staging: Stage 1 = creatinine rise 1.5-1.9x baseline or UO <0.5 mL/kg/hr for 6-12 hours; Stage 2 = 2.0-2.9x; Stage 3 = 3.0x or creatinine >4.0 mg/dL or RRT initiation.
Diagnosis & workup
Diagnostics & workup: - Monitor serum creatinine trends (rising creatinine is hallmark of AKI) - Calculate fractional excretion of sodium (FENa): <1% = prerenal, >2% = intrinsic ATN - Assess urine sediment: bland = prerenal; muddy brown granular casts = ATN; RBC casts = glomerulonephritis; WBC casts = pyelonephritis - Monitor BUN:creatinine ratio (>20:1 suggests prerenal) - Order renal ultrasound to evaluate for hydronephrosis (postrenal obstruction) - Monitor potassium, phosphorus, bicarbonate, calcium - Assess urine output (oliguria <0.5 mL/kg/hr or anuria <100 mL/day)