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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
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.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
IgA nephropathy, the most common primary glomerulopathy worldwide, is a disorder of B-cell origin with kidney pathology characterized by mesangial IgA-containing immune complex accumulation. At least 50% of patients progress to kidney failure or death within 10-20 years of diagnosis. Atacicept is a native human transmembrane activator, calcium-modulator and cyclophilin ligand interactor (TACI)-Fc fusion protein that inhibits two key immunoregulatory cytokines, B-cell activating factor (BAFF) and A proliferation-inducing ligand (APRIL), considered central to the pathophysiology of IgA nephropathy.
In this double-blind, placebo-controlled, multicenter, Phase 3 trial (ORIGIN 3), IgA nephropathy patients were randomized 1:1 to atacicept 150 mg or placebo, self-administered subcutaneously at home once weekly. The primary endpoint was percentage change from baseline at Week 36 in 24-hour urinary protein-to-creatinine ratio (UPCR) with secondary endpoints of change from baseline in galactose-deficient IgA1 (Gd-IgA1) and hematuria resolution. Safety was also evaluated.
This prespecified interim analysis at Week 36 included 203 patients (atacicept n=106; placebo n=97). Nearly all patients (99.5%) were receiving a stable dose of maximally-tolerated renin-angiotensin system inhibitors, and 53.2% (55.7% in the atacicept group; 50.5% in patients on placebo) were on a stable dose of sodium-glucose transporter 2 inhibitors at baseline. Atacicept treatment resulted in a geometric mean reduction of 45.7% in UPCR vs. a 6.8% reduction with placebo (treatment difference: 41.8% [95% CI, 28.9% to 52.3%; P<0.001]) (Figure A) that was maintained across subgroups of patients, regardless of baseline characteristics). Serum Gd-IgA1 was reduced by 68.3% from baseline in the atacicept group, compared with 2.9% in the placebo group (Figure B). Of the 122 patients who had a baseline dipstick hematuria of ≥1+, 81.0% of those treated with atacicept achieved hematuria resolution compared with 20.7% of those receiving placebo (Figure C). Adverse events were similar between atacicept and placebo groups.
In this prespecified interim analysis, atacicept treatment resulted in a significant reduction in proteinuria compared with placebo at Week 36 in patients with IgA nephropathy as well as reductions in Gd-IgA1, and hematuria resolution. The results demonstrate the potential for atacicept to address the underlying pathophysiology of IgA nephropathy and provide a targeted, disease-modifying therapy.
This abstract was also presented at the ASN Kidney Week 2025 congress.
