Abstract: TH-PO0519
Distant Triggers of IgAN
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
- Vaidya, Neha Vijay, University of California San Francisco, San Francisco, California, United States
- Sosa, Piera A., University of California San Francisco, San Francisco, California, United States
- Laszik, Zoltan G., University of California San Francisco, San Francisco, California, United States
- Showers, Christopher R., University of California San Francisco, San Francisco, California, United States
Introduction
IgA Nephropathy (IgAN) has a broad range of clinical presentations. Patients with psoriasis and prior exposure to TNF-alpha inhibitors are at increased risk of IgAN. Consequently, treatment of IgAN in these patients requires management of secondary triggers.
Case Description
A 48 year old male with plaque psoriasis and psoriatic arthritis presents for evaluation of rising creatinine with hematuria and proteinuria. He received adalimumab from 2021-2023 and then transitioned to secukinumab given concerns for worsening fatigue due to adalimumab. Both his skin and joint disease have been well controlled. His baseline creatinine was 1.0-1.1, though rose to 1.4 starting 8/2025. Urine studies were notable for microscopic hematuria and proteinuria with UACR 161 mg/g and UPCR of 214 mg/g. SPEP and complement levels were unremarkable. There were no clinical signs of infection. Renal biopsy demonstrated mesangial expansion, cellular crescents, and immune complex deposition of IgA with C3; M1 E0 S0 T0 C1. There were no subepithelial deposits and no significant interstitial fibrosis or tubular atrophy.
This patient’s subacute presentation with little disease chronicity raised concern for a secondary cause of IgAN. Given stable psoriatic disease we speculate that IgAN may have been precipitated by adalimumab exposure. The patient continues to remain on secukinumab with avoidance of TNF-alpha inhibitors; and was started on sparsentan to aid in reduction of glomerular pressure.
Discussion
In an era of developing therapies, recognizing secondary causes of IgAN remains essential to address IgAN pathogenesis. In particular, control of primary inflammatory conditions and cessation of drugs that may exacerbate IgAN are necessary for management.
Teaching points:
-TNF-alpha inhibitors can lead to secondary IgAN even after discontinuation of medication.
-Consider secondary causes of IgAN in patients with inflammatory/autoimmune conditions and extensive drug exposures.
-Treatment of secondary IgAN involves addressing underlying triggers in addition to standard treatments targeting IgAN pathogenesis.