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Kidney Week

Abstract: PUB382

Crescentic IgA Nephropathy: Levamisole-Induced?

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Rifai, Zeyad Jandali, Southern Illinois University School of Medicine, Springfield, Illinois, United States
  • Rowe, Heather, Southern Illinois University School of Medicine, Springfield, Illinois, United States
  • Ramani, Nirali Babubhai, Southern Illinois University School of Medicine, Springfield, Illinois, United States
Introduction

Immunoglobulin A (IgA) nephropathy is the most common primary glomerulonephritis (GN) worldwide and results from galactose- deficient IgA1 deposition within mesangial cells triggering an autoimmune response. Less than 10% of cases present as rapidly progressive GN. Levamisole is a cocaine adulterant, classically associated with ANCA vasculitis, that has a variable pattern of immunologic disturbance of renal significance.

Case Description

A 58-year- old female with a history of IV drug-use induced hepatitis C, with a negative viral load for two years following glecaprevir-pibrentasvir therapy, presented to the hospital with one month of intermittent hematuria, vague abdominal discomfort, malaise, and bilateral lower extremity worsening large violaceous plaques with early signs of ulceration. She admitted to frequent cocaine use and heavy NSAID usage for her abdominal discomfort and malaise but was unable to quantify either substance. Serum creatinine was at her baseline of 1.0 mg/dL, however, her urine protein creatinine ratio was 25 mg/mg with 219 RBC/HPF. Serologic, antiphospholipid, celiac and hepatitis workup were completely unremarkable. There was significant concern for ANCA negative levamisole induced vasculitis in the setting of cocaine usage versus NSAID induced glomerulonephritis. A renal biopsy was obtained revealing mesangial staining for IgA, IgM, C3 with diffuse mesangial hypercellularity, with 77% of glomeruli with fibrocellular crescents. This represented an Oxford classification of M1, E0, S0, T0, C2. The patient was discharged on losartan, moderate dose prednisone and cyclophosphamide. Outpatient follow-up with notable improvement in proteinuria and hematuria, she currently has preserved renal function with a creatinine of 1.0 mg/dL.

Discussion

This unusual presentation of possible levamisole induced crescentic IgA nephropathy (cIgAN) is confounded by the possibility of superimposed ANCA negative levamisole induced vasculitis as the underlying mechanism for the crescentic glomerular injury. There is no literature on levamisole induced cIgAN, we aim to share the first potential association between levamisole and development of cIgAN based on histologic findings. Alternatively, the cIgAN may be the outcome of hepatotoxicity resu from the resolved hepatitis C infection, however the patient’s presentation and the timeline is more suggestive of a levamisole induced process.