A 50-year-old diabetic patient in ICU develops oliguria after contrast-enhanced CT (CIAKI). Creatinine rises by 1.8 mg/dL (>0.3 mg/dL within 48 hours). On further assessment, urine sodium is 8 mmol/L, FENa is 0.4%, and urine osmolality is 620 mOsm/kg. These findings indicate:
- A Pre-renal AKI — tubular concentrating ability is preserved ✓
- B Intrinsic AKI (acute tubular necrosis) — FENa >1% expected
- C Post-renal AKI — obstruction is causing these values
- D Chronic kidney disease exacerbation — creatinine rise insufficient for AKI
Explanation
Low urine sodium (<20 mmol/L), FENa <1%, and high urine osmolality (>500 mOsm/kg) indicate intact tubular function and sodium reabsorption, consistent with pre-renal physiology (decreased renal perfusion). In acute tubular necrosis, tubular cells lose concentrating ability giving FENa >2% and urine osmolality <350 mOsm/kg. CIAKI can cause ATN in some cases but mild early contrast nephropathy can also present with pre-renal pattern.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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