A 65-year-old diabetic woman on ACE inhibitor develops AKI after starting an NSAID for joint pain. Serum creatinine rises from 1.1 to 2.9 mg/dL. FENa is 0.3%. Urine microscopy shows hyaline casts only. What is the mechanism of NSAID-induced AKI in this setting?
- A Direct tubular toxicity causing acute tubular necrosis
- B Allergic interstitial nephritis with eosinophiluria
- C Inhibition of prostaglandin-mediated afferent arteriolar dilation, reducing GFR in a prostaglandin-dependent state ✓
- D Renal papillary necrosis due to medullary ischaemia
Explanation
In patients with compromised renal perfusion (diabetes, ACE inhibitor use, or pre-existing CKD), baseline GFR is maintained by prostaglandin-mediated afferent arteriolar vasodilation. NSAIDs inhibit COX enzymes, reducing prostaglandin synthesis and precipitating afferent vasoconstriction, causing haemodynamic (pre-renal) AKI. This explains the FENa <1% and hyaline casts (no tubular necrosis). Acute tubulointerstitial nephritis (allergic) typically occurs after weeks of NSAID use and shows eosinophiluria and white cell casts. Papillary necrosis is a chronic complication of analgesic nephropathy.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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