IgA nephropathy is the most prevalent primary glomerular disease, often progressing to end-stage kidney disease (ESKD). Complement activation leads to glomerular damage by immune complex deposition and release of proinflammatory cytokines. Terminal complement inhibition specifically targets the pathophysiology of IgA nephropathy and may provide improved renal outcomes.
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Barratt et al. (2024) studied this question.
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