Abstract: SA-PO0910
IgA Vasculitis Triggered by Semaglutide
Session Information
- Glomerular Case Reports: ANCA, IgA, IgG, and More
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Hoteit, Mayssaa, Bridgeport Hospital, Bridgeport, Connecticut, United States
- Worwa, Stefanie, University of Minnesota Medical School, Minneapolis, Minnesota, United States
- Koubar, Sahar, University of Minnesota Medical School, Minneapolis, Minnesota, United States
Introduction
IgA vasculitis (IgAV) is an immune complex-mediated small-vessel vasculitis marked by IgA1-dominant deposits. Its pathogenesis is unclear, but genetic, environmental, and drug-related factors are implicated. Drug-induced IgAV remains challenging to diagnose. Semaglutide, a GLP-1RA used in T2DM and obesity, is generally well tolerated, but emerging data suggest possible associations with rare immune-mediated diseases. Two cases of leukocytoclastic vasculitis (LCV) have been reported in association with semaglutide. We present the third case of LCV, with biopsy-proven IgA nephropathy, likely triggered by semaglutide.
Case Description
A 65-year-old woman with obesity, hypertension, and hyperlipidemia developed a painful, burning, and pruritic purpuric rash on her lower extremities two weeks after initiating semaglutide and one week following influenza vaccination. Skin biopsy showed LCV. Systemic symptoms were absent. Prednisone 40 mg daily was started with gradual improvement. Extensive workup including hepatitis B/C, HIV, ANA, ANCA, cryoglobulins, and complement levels was unremarkable. Urinalysis revealed microscopic hematuria and uPCR was 1.4 g/g. Her eGFR was preserved. Kidney biopsy showed IgA nephropathy. She was initiated on a prednisone taper, lisinopril, and later started on empagliflozin, with complete resolution of the proteinuria and the rash.
Discussion
This case likely illustrates a semaglutide-associated IgA vasculitis with kidney involvement. The close temporal relationship to the drug initiation, negative workup for secondary causes, and sustained remission after drug discontinuation strongly support a causal link. GLP-1 receptors are present on various cell types, including neutrophils. Previous studies have suggested that semaglutide may influence neutrophil migration. This is especially relevant in LCV, where vascular injury is driven by neutrophil infiltration and the subsequent release of proteolytic enzymes. As GLP-1RA use expands, clinicians should be aware of this potential, albeit rare, complication.