A 55-year-old woman on chronic NSAIDs and an ACE inhibitor for hypertension undergoes coronary angiography with iodinated contrast. Twenty-four hours later, her serum creatinine rises from 1.0 to 2.4 mg/dL. Urinalysis shows bland sediment with no casts. Urine sodium is 8 mEq/L, fractional excretion of sodium (FeNa) is 0.3%. Which type of AKI does this represent?

• A Intrinsic AKI due to contrast nephropathy (acute tubular injury)
• B Pre-renal AKI due to effective volume depletion ✓
• C Post-renal AKI due to urinary obstruction
• D Intrinsic AKI due to acute interstitial nephritis from NSAIDs

Explanation

FeNa < 1% and urine sodium < 20 mEq/L with a bland sediment suggest pre-renal physiology (intact tubular sodium-conserving response). NSAIDs inhibit prostaglandin-mediated afferent arteriolar dilation and impair the compensatory response to reduced renal perfusion; ACE inhibitors blunt efferent arteriolar vasoconstriction, further reducing GFR. Together they predispose to hemodynamically mediated (functional/pre-renal) AKI in the setting of contrast administration. Contrast nephropathy produces ATN with granular muddy-brown casts and FeNa typically > 1%.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.