Abstract: TH-PO0530
Lucio Phenomenon with IGAN Presenting as AKI in Untreated Lepromatous Leprosy: A Case Report
Session Information
- Glomerular Diseases: IgAN, IgA Vasculitis, and More
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Mokariya, Dipak Ramesh, Maulana Azad Medical College, New Delhi, DL, India
- Vanteru, Abinay Siva kumar Reddy, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
- Johari, Vardan, Maulana Azad Medical College, New Delhi, DL, India
- Anand, Jaspreet Singh, Maulana Azad Medical College, New Delhi, DL, India
- Mandal, Aritra, Maulana Azad Medical College, New Delhi, DL, India
Introduction
Lucio phenomenon is a rare necrotizing vasculopathy observed in untreated diffuse lepromatous leprosy and represents a dermatologic emergency. Renal involvement in leprosy is well described and includes immune complex mediated glomerulonephritis, amyloidosis, and drug-induced nephrotoxicity. However, biopsy-proven IgA nephropathy in association with Lucio phenomenon (type 2 lepra reaction) is exceedingly rare, with very few reported cases. We describe a unique case of inadequately treated multibacillary lepromatous leprosy presenting with Lucio phenomenon and acute kidney injury secondary to biopsy-proven IgA nephropathy
Case Description
A 55-year-old woman presented with fever, painful erythematous angulated plaques over the extremities, and oliguria. She had a prior history of inadequately treated leprosy. Physical examination revealed madarosis, thickened peripheral nerves, hepatosplenomegaly, and ulcerative plaques, suggestive of Lucio phenomenon. Slit-skin smear confirmed multibacillary leprosy. Laboratory evaluation showed elevated blood urea nitrogen (126 mg/dL) and serum creatinine (3.0 mg/dL), along with low complement C3 levels. Urinalysis revealed active sediment with 3+ proteinuria, dysmorphic red blood cells, and granular casts; 24-hour urine protein was 2.4 g/day. After exclusion of other etiologies, a renal biopsy was performed, demonstrating enlarged glomeruli with mesangial expansion, hypercellularity, and acute tubular injury. Immunofluorescence revealed mesangial deposits of IgA (3+), IgG (1+), and C3 (2+), consistent with IgA nephropathy.
The patient was treated with systemic corticosteroids and multidrug therapy (MDT) for leprosy, along with supportive care. She achieved complete renal remission within one month, with normalization of kidney function and urinalysis, and partial resolution of skin lesions. Corticosteroids were gradually tapered, and she remains on MDT.
Discussion
This case highlights a rare association of IgA nephropathy with Lucio phenomenon presenting as acute kidney injury in untreated lepromatous leprosy. Early recognition and a multidisciplinary approach, including MDT and corticosteroid therapy, can lead to favorable outcomes in both renal and dermatologic manifestations