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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.
Dysregulation of the gut-kidney axis is believed to play a pivotal role in the pathogenesis of immunoglobulin A nephropathy (IgAN). Genome-wide association studies have identified multiple risk alleles associated with development of IgAN, many of which are involved in the synthesis of immunoglobulin A (IgA) within the gut-associated lymphoid tissue (GALT). Furthermore, IgA generated at mucosal surfaces shares many of the physicochemical properties characteristic of mesangial IgA deposits and is enriched in circulating IgA immune complexes. Nefecon is a targeted-release budesonide formulation that delivers high, localized concentrations of budesonide to the terminal ileum of the GALT, reducing the production of pathogenic forms of IgA. Biomarker analyses from the Phase 2 NEFIGAN study supported the disease-modifying activity of nefecon through the GALT (Wimbury D, et al. Kidney Int. 2024;105:381-388). In this study, we evaluated the effect of nefecon on serum biomarkers of GALT activity using samples from the Phase 3 NefIgArd trial.
NefIgArd was a double-blind, randomized, placebo-controlled clinical trial in patients with IgAN at high risk of progressive kidney disease despite optimized supportive care. The trial comprised a 9-month treatment period with either placebo or nefecon 16 mg/day (n=182 for each arm) on top of optimized supportive care, followed by a 15-month off-treatment period on optimized supportive care alone. Treatment with nefecon led to a reduction in proteinuria at 9 months (p=0.0005) and a reduction in eGFR decline at 24 months (p<0.0001) compared with placebo. Serum for biomarker evaluation was collected at baseline and months 3, 6, and 9 post-randomization. Levels of APRIL, BAFF, sBCMA, CCL11, CCL13, CCL19, CCL20, CXCL5, CXCL6, CXCL13, IL18Bpa, sCD23, sCD27 and sCD30 (see table footnote for definitions) were measured in these serum samples from 223 participants using Luminex and ELLA technologies. Comparisons between placebo- and nefecon-treated groups were made at each study time point using robust regression with multiple imputations, with a significance threshold set at p<0.05.
Treatment with nefecon 16 mg/day resulted in significant changes in the levels of a number of cytokines, chemokines and soluble lymphocyte receptors (Table). Protein-protein interaction and pathway analysis confirmed that these proteins were closely involved in the production of IgA within the GALT.
Consistent with observations from the Phase 2 NEFIGAN study, we have now validated changes in a range of serum biomarkers of GALT function, indicating that nefecon directly modulates activity of the mucosal immune system of the small intestine, and impacts upon key proteins involved in the regulation of IgA synthesis within the GALT. We previously reported that in these same participants, treatment with nefecon significantly reduced serum levels of galactose-deficient IgA1 (Gd-IgA1), anti–Gd-IgA1 immunoglobulin G (IgG) and IgA-IgG immune complexes. Collectively these data support a disease-modifying role for nefecon in the treatment of IgAN.
