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Initial findings suggest that complement-targeted treatments could help with IgA.

Kevin Anderson

IgA nephropathy (IgAN) is the most frequent kind of primary glomerulonephritis and a leading cause of end-stage renal disease around the world. The diagnosis requires a kidney biopsy, with routine immunofluorescence microscopy demonstrating dominant or co-dominant IgA immunodeposits, generally with complement C3, and occasionally IgG and IgM. IgA nephropathy shortens life by more than a decade and causes kidney failure in more than half of patients within a year of diagnosis. Complement plays a key role in the aetiology of IgA nephropathy, according to mounting clinical, genetic, and biochemical evidence. The presence of C3 distinguishes IgA nephropathy from glomerular IgA deposition in the asymptomatic stage. In renal biopsy specimens, markers indicating the activation of the alternative and mannan-binding lectin (MBL) pathways are linked to disease activity and portend a worse renal outcome. In IgA nephropathy, complement proteins in the circulation have also been studied and found to have predictive relevance. IgA nephropathy-related loci have recently been discovered through genetic investigations. Genes encoding products involved in complement control and interaction with immune complexes are found within these regions. These findings point to the complement cascade as a viable therapy target for chronic renal disease. Recent case reports demonstrating the efficacy of the humanised anti-C5 monoclonal antibody eculizumab support this notion, but more research into the involvement of complement in IgA nephropathy is needed to guide future treatment strategies.