Acute Kidney Injury
Nephrology
Illness script · Nephrology
Acute Kidney Injury
Abrupt decline in renal function (↑Cr ≥0.3 mg/dL in 48h or ≥1.5× baseline in 7d) causing azotemia and fluid/electrolyte dysregulation.
This illness script for Acute Kidney Injury covers predisposing factors, classic presentation, mechanism, workup, management, and the clinical pivots that separate it from look-alikes—written for USMLE Step 1 and clerkship reasoning.
01
Predisposing factors
- Pre-renal: hypovolemia, heart failure, hepatorenal syndrome
- Intrinsic-renal: nephrotoxins (NSAIDs, aminoglycosides, contrast), ATN, glomerulonephritis
- Post-renal: BPH, malignancy, nephrolithiasis causing obstruction
- Risk factors: CKD, DM, elderly, ICU admission, sepsis
02
Presentation
- Often asymptomatic; detected on labs (rising Cr/BUN)
- Oliguria (<400 mL/day) or anuria (<100 mL/day) in severe cases
- Volume overload: edema, pulmonary crackles, hypertension
- Uremic symptoms (late): nausea, asterixis, pericardial friction rub, encephalopathy
- Hyperkalemia → peaked T-waves, arrhythmia (EKG finding)
- Post-renal: colicky flank pain, distended bladder, bilateral hydronephrosis on US
03
Pathophysiology
- Pre-renal: ↓effective circulating volume → ↓GFR without tubular damage (reversible)
- ATN (most common intrinsic): ischemia or nephrotoxin → tubular epithelial cell death → cast obstruction + back-leak
- Post-renal: bilateral obstruction raises tubular pressure → ↓GFR; prolonged obstruction → irreversible fibrosis
- All causes → ↓GFR → BUN/Cr rise, hyperkalemia, metabolic acidosis, fluid overload
04
Diagnostics
- Urine studies: FENa <1% pre-renal (tubules intact), FENa >2% ATN
- UA: muddy brown granular casts = ATN; RBC casts = glomerulonephritis; WBC casts = pyelonephritis/interstitial nephritis
- BUN:Cr ratio >20:1 suggests pre-renal; <15:1 suggests intrinsic
- Renal US: first-line imaging to rule out obstruction (hydronephrosis)
- Renal biopsy: gold standard for intrinsic causes when etiology unclear; not needed for ATN
05
Management
- Pre-renal: IV fluids (isotonic saline or albumin in cirrhosis); remove offending agents
- ATN: supportive — optimize hemodynamics, hold nephrotoxins, strict I&O; NO role for diuretics to convert oliguric ATN
- Post-renal: relieve obstruction (Foley, ureteral stent, nephrostomy tube) urgently
- Hyperkalemia: calcium gluconate (stabilize membrane), insulin + dextrose, kayexalate, dialysis
- Indications for emergent dialysis (AEIOU): Acidosis, Electrolytes (K), Intoxication, Overload (fluid), Uremia (pericarditis, encephalopathy)
06
Clinical pivots
How to separate this script from the look-alikes that show up on exams and on the wards.
CKD (Chronic Kidney Disease)
CKD: ↑Cr >3 months + small echogenic kidneys on US; AKI is acute (<48h–7d) with normal or near-normal prior baseline
Pre-renal azotemia vs. ATN
Pre-renal: FENa <1%, BUN:Cr >20, UA normal, rapidly reverses with fluids; ATN: FENa >2%, muddy brown casts, does NOT rapidly reverse
Acute interstitial nephritis (AIN)
AIN: drug exposure (NSAIDs, PCN, PPIs) + WBC casts + eosinophiluria + rash/fever triad; responds to steroids
Hepatorenal syndrome
HRS: AKI in cirrhosis/liver failure with normal UA, FENa <1%, no improvement with 1.5L albumin challenge
Keep reading
Full library- Acute Decompensated Heart FailureSudden worsening of HF symptoms causing fluid overload and/or low cardiac output requiring urgent hospitalization.
- Acute PancreatitisAcute inflammation of the pancreas due to premature activation of digestive enzymes, causing autodigestion and systemic inflammation.
Educational use only. This illness script is a study framework, not medical advice. Confirm decisions with current guidelines and your clinical supervisors.