Abstract: TH-PO0516
Hydralazine-Induced IgA Vasculitis in a Dialysis-Dependent Patient with Primary IgAN: A Case with Positive Rechallenge
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
Author
- Sharma, Sona, NYC Health + Hospitals Queens Hospital Center, Jamaica, New York, United States
Introduction
IgA vasculitis (IgAV) is a small-vessel vasculitis characterized by IgA immune complex deposition affecting skin, joints, GI tract, and kidneys. [1] IgA nephropathy (IgAN) represents the kidney-limited form; both are histopathologically indistinguishable, representing a disease spectrum. [1] Drug-induced IgAV in ESRD patients with underlying IgAN is rarely reported.
Case Description
A 51-year-old woman with ESRD from IgA nephropathy on hemodialysis presented with fatigue, abdominal pain, and melena. History included hypertension treated with hydralazine, diabetes, and heart failure. Labs showed hemoglobin 6.6 g/dL and thrombocytopenia.
On day 3, she developed palpable purpura on bilateral lower extremities with arthralgias. Skin biopsy confirmed leukocytoclastic vasculitis with IgA, IgM, and C3 deposition. Serologies revealed ANA >1:2560 with negative ANCA which was an atypical finding, as hydralazine-associated vasculitis typically shows dual ANA/ANCA positivity. [4]
Symptoms improved after hydralazine discontinuation but recurred upon inadvertent re-exposure, confirming drug causation. High-dose methylprednisolone led to rapid improvement. At one month, complete resolution was achieved.
Discussion
This case demonstrates drug-induced evolution from IgAN to systemic IgAV in ESRD. The classic IgAV tetrad - purpura, arthralgias, GI involvement, and nephritis was present. [2] Inadvertent rechallenge provided compelling causality evidence. Hydralazine causes vasculitis through haptenization and MPO modification generating pathogenic autoantibodies. [5-6] The atypical serologic profile (high ANA without ANCA) may reflect underlying IgAN pathophysiology modifying the immune response. [4]
Drug discontinuation with corticosteroids achieved complete resolution without maintenance immunosuppression, consistent with favorable prognosis of drug-induced versus idiopathic vasculitis.
Acknowledgment
1) Eknoyan G, et al. KDIGO 2025 IgAN/IgAV Guideline. 2025.
2) Kumar B, et al. Semin Arthritis Rheum. 2018;48(2):283-287.
3) Castañeda S, et al. J Clin Med. 2024;13(21):6621.
4) Rasmussen C, et al. Autoimmunity Reviews. 2021;20(1):102707.
5) Xi G, et al. J Clin Invest. 2025;135(8):e178813.
6) Santambrogio L. J Clin Invest. 2025;135(8):e191587.
7) Ford JA, Monach PA. Lancet Rheumatol. 2019;1(4):e247-e256.