Triple-Crown Kidney Injury in a Patient with Diabetes

Introduction: Diabetic kidney disease (DKD) progresses slowly; AKI or nephrotic proteinuria signals superimposed injury. Secondary FSGS or malignant-HTN TMA occurs in <5% of DKD biopsies; coexistence with NSAID-related chronic interstitial nephritis is unreported. Case Description: A 59-year-old man with type 2 diabetes, six months off all medications, and daily NSAIDs presented in hypertensive crisis (MAP 167) with creatinine 5.1 mg/dL, albumin 2.6 g/dL, and 10 g/d proteinuria; urinalysis showed microscopic hematuria, and kidneys were normal in size. Pathology (Figures 1-2) guided care: NSAID withdrawal and staged BP control lowered creatinine to 2.3 mg/dL and proteinuria to 3 g/d in four weeks, avoiding dialysis at that time. Discussion: Biopsy diabetic patients with atypical AKI or nephrotic proteinuria to identify reversible lesions; targeted treatment of metabolic (nodular diabetic GS), hemodynamic (malignant-HTN TMA), and toxic (NSAID-induced CIN) insults may reverse compound kidney injury.Glomerular Composite A) PAS: diffuse nodular sclerosis. B) Silver: GBM thickening. C) Trichrome: segmental scar (secondary FSGS). D) EM: widespread podocyte effacement.Vascular/Interstitial Composite A) H&E: arteriolar fibrinoid necrosis/onion-skinning (HTN-TMA). B) H&E: eosinophil-rich CIN. C) Trichrome: interstitial fibrosis + acute tubular injury.