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It highlights the diagnostic challenges posed by overlapping features with hemolytic uremic syndrome and membranoproliferative glomerulonephritis, as well as the difficulty in distinguishing complement overactivation from true regulatory failure. Key mechanisms of complement activation and the role of regulatory proteins are discussed, along with operative and clinical risk factors such as ischemia-reperfusion injury, delayed graft function, viral infections, and monoclonal gammopathy. The review describes the histopathologic spectrum of C3G in the allograft and underscores the importance of early protocol biopsies for timely detection. Management strategies include conservative measures, nonspecific immunosuppression, and emerging complement-targeted therapies. Recent Food and Drug Administration approvals of iptacopan and pegcetacoplan represents major advances. 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