A patient develops renal papillary necrosis after chronic NSAID use. The analgesic nephropathy is primarily attributed to inhibition of which prostaglandin responsible for maintaining medullary blood flow?
- A PGE2 and PGI2 (prostacyclin) synthesised by medullary interstitial cells ✓
- B TXA2 produced by renal collecting duct principal cells
- C PGF2-alpha synthesised by juxtaglomerular apparatus cells
- D Leukotriene B4 produced by renal cortical macrophages
Explanation
The renal medulla, which operates at the edge of hypoxia due to its countercurrent architecture, depends critically on locally synthesised PGE2 and prostacyclin (PGI2) to maintain medullary blood flow by causing vasodilation of the vasa recta. NSAIDs, by inhibiting COX-1 and COX-2 in medullary interstitial cells, reduce these prostaglandins, cause unopposed vasoconstriction of the vasa recta, medullary ischaemia, and ultimately renal papillary necrosis with chronic use. Thromboxane A2 (TXA2) is vasoconstricting and pro-thrombotic; its inhibition by NSAIDs is not the nephropathy mechanism. Leukotrienes are not primarily involved in medullary blood flow regulation.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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