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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.
Aberrant activation of the alternative complement pathway is increasingly recognised as a central driver of IgA nephropathy (IgAN). While most prior work has focused on circulating complement components or factor H–related (FHR) protein levels, the clinical significance of CFHR gene variants remains insufficiently defined. Characterising their phenotypic and pathological correlates could unravel disease heterogeneity, refine risk stratification, and inform the design of precision complement-targeted interventions.
We retrospectively analysed 142 patients evaluated for complement-mediated kidney disease at a tertiary nephrology centre in India between January 2021 and April 2025. All underwent CFHR gene copy-number and sequence analysis using multiplex ligation-dependent probe amplification and/or targeted next-generation sequencing. Among these, 23 biopsy-proven IgAN cases were systematically examined for genotype–phenotype correlations, complement biomarker signatures, histopathological severity, and renal outcomes. Clinical and pathological variables were compared between patients with and without CFHR alterations.
Pathogenic or likely pathogenic CFHR variants were identified in 48% (11/23) of IgAN cases, most commonly CFHR1/3 deletions (n = 6) and CFHR5 variants (n = 3). Patients carrying CFHR variants exhibited a markedly higher prevalence of thrombotic microangiopathy-like injury (44% vs. 11%, p = 0.018), increased crescent formation (39% vs. 13%, p = 0.032), and a greater requirement for kidney replacement therapy during follow-up (36% vs. 9%, p = 0.041). Complement abnormalities — including reduced serum C3 and anti-factor H antibody positivity — were significantly enriched among mutation carriers. Kaplan–Meier survival analysis demonstrated inferior kidney survival in the mutation-positive cohort (log-rank p = 0.008).
CFHR gene alterations define a clinically and histologically distinct subtype of IgAN characterised by excessive complement activation, microangiopathic injury, and accelerated progression to kidney failure. Incorporating CFHR genetic screening into diagnostic workflows could enable early identification of high-risk patients and guide precision therapy. These findings also establish a biological rationale for stratifying patients in future clinical trials of complement inhibitors, potentially transforming the therapeutic landscape of IgAN.
