Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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.
A proliferation-inducing ligand (APRIL) plays a key role in the pathogenesis of immunoglobulin A (IgA) nephropathy, a progressive immune-mediated chronic kidney disease characterized by the deposition of Gd-IgA1–containing immune complexes in the glomerular mesangium. Sibeprenlimab, a humanized IgG2 monoclonal antibody, selectively binds to and blocks the biological actions of APRIL. In the Phase 2 ENVISION trial (NCT04287985), sibeprenlimab reduced proteinuria, stabilized eGFR, suppressed serum APRIL, and decreased Gd-IgA1 levels in people with IgA nephropathy. In a prespecified interim analysis of the ongoing VISIONARY pivotal Phase 3 clinical trial (NCT05248646), sibeprenlimab led to a 51.2% (P<0.0001) placebo-adjusted reduction in 24-hour urine protein-creatinine ratio at 9 months and markedly reduced Gd-IgA1 and APRIL compared with placebo at 48 weeks. The impact of sibeprenlimab at the kidney tissue level remains to be characterized. VISOR (NCT06740526) aims to evaluate the anti-APRIL effect of sibeprenlimab on immune-mediated drivers of disease activity in kidney biopsies.
VISOR is a Phase 2b, multicenter, open-label, repeat kidney biopsy, single-arm trial of sibeprenlimab in adults (aged ≥18 years) with IgA nephropathy (Figure). Eligible patients will receive sibeprenlimab 400 mg subcutaneously every 4 weeks for up to 2 years. Patients must have a kidney biopsy confirming IgA nephropathy diagnosis (key inclusion and exclusion criteria are listed in Table). If adequate tissue is available from a diagnostic biopsy collected within 24 weeks of the anticipated start of treatment with sibeprenlimab, the diagnostic biopsy may serve as the baseline biopsy; alternatively, a baseline research biopsy may be performed. Repeat protocol biopsies are obtained at week 52 and, for patients continuing into year 2, week 104. The use of nonimmunosuppressant background therapy for IgA nephropathy (eg, ACE inhibitors, angiotensin receptor blockers, mineralocorticoid receptor antagonists, SGLT2 inhibitors, and endothelin receptor antagonists) is permitted at the discretion of investigators.
Approximately 50 patients will be enrolled across approximately 18 global sites. The primary endpoint is the change from baseline to week 52 in glomerular IgA deposition in kidney tissue, assessed by immunofluorescence, as a measure of the underlying disease pathogenesis. The secondary endpoint is to assess the ongoing safety of sibeprenlimab. Exploratory objectives include evaluating additional changes in kidney tissue, including components of the MEST-C classification, a validated predictor of risk of progression and long-term renal outcomes; Gd-IgA1 deposition; complement factor deposition and CD68+ immune cells as markers of immune activation; and spatial transcriptomics. Exploratory blood and urine biomarkers relevant to IgA nephropathy pathophysiology will also be assessed.
VISOR will explore the histologic and cellular changes following sibeprenlimab treatment in patients with IgA nephropathy. These findings are expected to expand our mechanistic understanding of the effect of APRIL inhibition on histopathological changes in IgA nephropathy.
