Leptospirosis-Induced AKI with Unique Glomerular Findings: A Case of Recovery from Dialysis-Dependent AKI with Steroid Therapy

Introduction: Leptospirosis is a zoonotic disease that commonly causes AKI, typically manifesting as acute tubular necrosis and interstitial nephritis. We present a case of severe leptospirosis-associated AKI with distinctive glomerular findings that demonstrated remarkable recovery following steroid therapy. Case Description: A 61-year-old male marathon runner with CKD stage 3a (baseline SCr 1.3-1.5mg/dL) presented with malaise, nausea, vomiting, and bilateral lower extremity myalgia after sustaining a foot laceration in Hawaii with exposure to mongoose habitats. Laboratory evaluation revealed rhabdomyolysis (peak CK 12,000 U/L), leukocytosis, thrombocytopenia, hyponatremia, and rapidly worsening AKI (peak SCr 9.59mg/dL). Inflammatory markers were markedly elevated (ESR 81mm/hr, CRP 128.34mg/L) with striking nephrotic-range proteinuria (UPCR 16.2mg/mg). Despite fluid resuscitation and antibiotic therapy, progressive azotemia required hemodialysis. Serological testing confirmed leptospirosis. Kidney biopsy revealed active interstitial nephritis with lymphoplasmacytic infiltration, mild acute tubular necrosis with myoglobin casts, and unusual lamellar lipid/lipoprotein inclusions in the glomeruli on electron microscopy. Following steroid therapy, renal function improved, allowing discontinuation of hemodialysis. Four months later, steroids were successfully tapered with creatinine returning to baseline level (1.36mg/dL). Discussion: This case highlights unique aspects of leptospirosis-associated kidney injury, which is caused via immune-triggered AIN and tubular damage from bacterial LipL32 protein binding to renal epithelial cells. The unusual finding of glomerular lamellar lipid/lipoprotein inclusions was likely related to liver injury causing reduced LCAT synthesis and decreased cholesterol esterification. Evidence suggests patients with severe leptospirosis may develop persistent renal damage leading to progressive CKD, underscoring the importance of vigilant follow-up and targeted therapeutic interventions. The significant clinical improvement with corticosteroid therapy emphasizes the importance of promptly diagnosing AIN as a prominent etiology of leptospirosis-associated AKI, as steroids may be crucial for managing inflammation and recovery.