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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.
Recent studies have revealed that complement activation plays a key role in various forms of chronic proliferative glomerulonephritis (GN), and complement inhibitors targeting different points along the activation cascade have shown therapeutic efficacy. We previously reported that activated macrophages (MΦs) are critically involved in the pathogenesis of proliferative GN. In this study, we examined the role of complement receptor CR4 (CD11c/CD18)-positive activated MΦs in different types of proliferative GN.
Renal biopsy from patients diagnosed with proliferative GN, including IgA nephropathy (IgAN; n = 48), IgA vasculitis-associated nephritis (IgAV-N; n = 25), lupus nephritis (LN; grade III or higher; n = 18), and membranoproliferative GN (MPGN; n = 9). To evaluate glomerular accumulation of CD11c+ MΦ, multiplex immunostaining using antibodies against CD11c, CD68 (pan-macrophage marker), and CD86 (M1 activation marker) was performed, and the association with clinicopathological findings was analyzed.
The mean number of CD11c+ MΦs per glomerular cross-section was 1.1 in IgAN, 3.4 in IgAV-N, 9.0 in LN, and 3.9 in MPGN. A significant positive correlation was observed between CD11c+ MΦ count and both proteinuria (g/gCr) and the percentage of glomeruli exhibiting endocapillary proliferation across all disease groups (IgAN: p < 0.001; IgAV-N: p < 0.001; LN: p < 0.01; MPGN: p < 0.05). Notably, all CD11c+ MΦs were also positive for CD86, indicating M1-type activation.
CR4 (CD11c/CD18)+ MΦs exhibit M1-type inflammatory activation and are likely to contribute to the development of acute and active glomerular lesions in proliferative GN. These findings suggest that CR4+ MΦs may serve as potential therapeutic targets in complement-mediated glomerular diseases.
