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C3 glomerulopathy (C3G) and primary immune-complex membranoproliferative glomerulonephritis (IC-MPGN) are both prototypical complement disorders in which complement overactivation is the primary driver of disease. Complement is not the primary cause of disease in IgA nephropathy (IgAN); however, increasing evidence implicates complement as a secondary factor in kidney damage in this more complex, multifactorial disorder. The success of recent clinical trials using alternative pathway complement inhibitors in C3G, IC-MPGN, and IgAN pose questions as to how they should be used in the real world. We report the findings of the 2025 International Society of Nephrology Forum on Complement Therapeutics in C3G and IgAN, where a global panel of experts considered the current state of knowledge, identified areas of uncertainty, and proposed optimal solutions. Areas of uncertainty and areas for future research included how complement biomarkers, complement autoantibodies, genetics, and the kidney biopsy guide therapy. The current rationale for the use of complement inhibitors and their place within the current therapeutic landscape are discussed.
Kavanagh et al. (2026) studied this question.