Papillary necrosis

Papillary necrosis is acute ischemic necrosis of one or more renal papillae (medullary pyramids) due to impaired medullary blood supply and oxidative stress. Risk factors and causes: (1) NSAIDs (inhibit protective prostaglandin-mediated vasodilatation in vasa recta)—most common iatrogenic cause, especially in combination with dehydration; (2) Acute pyelonephritis—bacterial toxins and inflammatory cytokines damage papillae; (3) Sickle cell disease—sickling in hypoxic, hypertonic medulla causes vaso-occlusion; (4) Diabetes mellitus—hyperglycemia and renal failure promote ischemia; (5) Obstruction (ureteral stones, BPH)—increases intratubular pressure and reduces perfusion; (6) Cirrhosis with hepatorenal syndrome. Pathophysiology: reduced medullary perfusion (vasa recta closure) combined with hypoxia and oxidative stress triggers epithelial necrosis. The necrotic papillae may detach and slough into collecting system, potentially obstructing ureter (uric acid stones risk in severe cases). Presentation: acute flank pain (can be severe), hematuria (may be gross), fever (if infectious cause), and acute kidney injury (oliguria, elevated creatinine). Urinalysis shows hematuria, pyuria (if infected), and may contain papillary tissue fragments. Renal ultrasound or CT shows wedge-shaped areas of necrosis in renal medulla (papillary blunting or cavitation on imaging). Diagnosis is clinical + imaging (CT is most sensitive). Management: supportive care (hydration, analgesia), treat underlying cause (stop NSAIDs, treat infection with antibiotics, relieve obstruction), and manage AKI (fluid management, monitoring electrolytes). Risk of recurrence if causative factors persist. Chronic sequelae: repeated episodes of papillary necrosis can progress to chronic CTIN with papillary fibrosis and chronic kidney disease. Board relevance: suspect papillary necrosis in any patient with NSAIDs + dehydration + flank pain + AKI.