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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
IgA nephropathy (IgAN) has been characterized as an autoimmune disease in which IgA1-containing mesangial immunodeposits are derived from circulating immune complexes composed of galactose-deficient IgA1 (Gd-IgA1), the autoantigen, bound by Gd-IgA1–specific autoantibodies. According to the multi-hit pathogenesis model, overproduction of Gd-IgA1 represents the first hit and plays a central role in disease development. Associations between biologic agents and the onset of IgAN have been suggested, with cases reported following treatment with TNF-α inhibitors and immune checkpoint inhibitors, although the underlying mechanisms remain unclear. Here, we report a case of IgAN associated with risankizumab, an IL-23p19 monoclonal antibody, and discuss potential mechanisms in the context of previous reports on biologic agent–associated IgAN.
Case report: A 37-year-old man with a history of childhood tonsillectomy had no prior urinary abnormalities or renal dysfunction on routine screening. He was diagnosed with psoriatic arthritis in 2018 and treated sequentially with brodalumab, adalimumab, and ixekizumab, but these agents failed to adequately control his symptoms. Risankizumab was initiated in October 2023, leading to marked improvement in both joint and skin manifestations. Subsequently, renal function gradually declined: estimated glomerular filtration rate (eGFR) decreased from approximately 90–100 to 61.3 mL/min/1.73 m² by February 2025, accompanied by microscopic hematuria and proteinuria (urine protein-to-creatinine ratio 0.67 g/gCr).
Percutaneous renal biopsy revealed 74 glomeruli, with mesangial hypercellularity in 24, global sclerosis in 18, and endocapillary hypercellularity in 1; the tubulointerstitium showed mild fibrosis. Immunofluorescence showed granular mesangial deposition of IgA and C3, and deposition; Gd-IgA1 was co-localized with IgA also deposited in the mesangium. The diagnosis was IgAN, Oxford classification M1E1S0T0C0. Given stable control of psoriatic arthritis, risankizumab was continued, and two courses of high-dose intravenous corticosteroid pulse therapy were administered. eGFR improved to 70 mL/min/1.73 m², proteinuria resolved, and microscopic hematuria persisted.
Risankizumab, approved for psoriatic arthritis as well as Crohn’s disease and ulcerative colitis, primarily acts by inhibiting IL-23 and suppressing the Th17 axis. In this case, IL-23 pathway blockade may have induced a Th2-skewed immune response, potentially enhancing Gd-IgA1 production through the IL-4–STAT6 pathway and contributing to IgAN development. While IgAN has been reported in association with the IL-12/23p40 inhibitor ustekinumab, no previous case of risankizumab-associated IgAN has been described. Further accumulation of biologic-associated IgAN cases, including those involving IL-23p19 inhibition, may help elucidate the underlying disease mechanisms.
