A 50-year-old woman develops AKI (creatinine 3.2 mg/dL, baseline 0.9 mg/dL) after starting NSAIDs for arthritis. Urinalysis: no cells/casts, urine sodium 12 mEq/L, FENa 0.4%, urine osmolality 620 mOsm/kg. Which mechanism best explains this pattern?

• A NSAIDs cause direct tubular toxicity leading to acute tubular necrosis
• B NSAIDs trigger interstitial nephritis via T-cell-mediated hypersensitivity
• C NSAIDs cause thrombotic microangiopathy by inhibiting prostacyclin production
• D NSAIDs inhibit prostaglandin-mediated afferent arteriolar dilation, reducing GFR in states of heightened renal vasoconstriction dependence ✓

Explanation

This is prerenal AKI (FENa <1%, urine Na <20, high urine osmolality, no casts) caused by NSAID-induced afferent arteriolar vasoconstriction. Prostaglandins (PGE2, PGI2) normally maintain afferent arteriolar dilation in states where renal perfusion pressure is reduced (volume depletion, heart failure, cirrhosis). NSAID inhibition of COX enzymes removes this protective vasodilatory mechanism, causing GFR to fall. This is haemodynamic AKI, not tubular or interstitial. NSAID-induced AIN typically causes sterile pyuria, eosinophiluria, and non-oliguric AKI with different urine chemistry.

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

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Written and medically reviewed by the StethoPrep medical team.