AKI Classification: KDIGO Staging

KDIGO AKI criteria: creatinine rise ≥0.3 mg/dL within 48h, OR ≥1.5× baseline within 7 days, OR urine output <0.5 mL/kg/hr × ≥6h. Stage 1: Cr ×1.5–1.9 baseline or ↑≥0.3 within 48h. Stage 2: Cr ×2–2.9 baseline. Stage 3: Cr ×3 baseline or ≥4.0 mg/dL or RRT needed. BUN:Cr ratio: >20:1 suggests prerenal (concentrated urine, avid BUN reabsorption); <10–15:1 suggests intrinsic renal disease. Note: BUN elevation from GI bleed, corticosteroids, or high protein intake raises BUN independently of renal function — contextualize the ratio.

Prerenal AKI

Cause: reduced renal perfusion without intrinsic kidney damage. Etiologies: volume depletion (dehydration, GI losses, hemorrhage), low cardiac output (CHF, cardiogenic shock), vasodilation (sepsis, cirrhosis), renal vasoconstriction (NSAIDs block prostaglandin vasodilation; ACEi/ARBs block efferent arteriole constriction). Urine: high osmolality (>500 mOsm/kg), low urine Na (<20 mEq/L), FENa <1%. Treatment: fluid challenge — NS or LR bolus. If due to NSAIDs: stop NSAID. If hepatorenal syndrome (cirrhosis + prerenal AKI unresponsive to fluids): midodrine + octreotide + albumin, or terlipressin (if available) as bridge to liver transplant.

Intrinsic AKI

Glomerular: RBC casts (GN), proteinuria — treat underlying GN (immunosuppression for RPGN). Tubular (ATN — most common intrinsic): muddy brown casts, ischemia (sepsis, shock), nephrotoxins (aminoglycosides, contrast, cisplatin, myoglobin/rhabdomyolysis). FENa >2% (tubules cannot reabsorb Na). Treatment: remove offending agent, supportive — ATN is reversible in 1–3 weeks if cause removed. Interstitial (AIN): WBC casts + eosinophiluria, drug hypersensitivity (NSAIDs, PPIs, beta-lactams, sulfa), fever + rash + eosinophilia (triad in only 10%). Treatment: discontinue offending drug, steroids if no improvement. Vascular: TTP/HUS (schistocytes), renal artery stenosis.

Postrenal AKI and Indications for Dialysis

Postrenal: obstruction of urine flow. In hospitalized patients: foley catheter obstruction, neurogenic bladder. Outpatient causes: BPH (bilateral obstruction), bilateral ureteral stones, retroperitoneal mass, cervical cancer. Diagnosis: bladder ultrasound or catheter drainage for bladder outflow obstruction; renal ultrasound for hydronephrosis (bilateral for postrenal AKI). Treatment: relieve obstruction — catheter, stent, or percutaneous nephrostomy. Post-obstructive diuresis: watch for massive urine output and replace fluids/electrolytes. AEIOU indications for urgent dialysis: Acidosis (pH <7.1), Electrolytes (K+ >6.5 or refractory), Intoxication (methanol, ethylene glycol, lithium, salicylates), Overload (refractory pulmonary edema), Uremia (encephalopathy, pericarditis, bleeding).