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Multiple genetic and acquired defects involving plasma\u2010 and membrane\u2010associated proteins are probably necessary to impair the protection of host tissues and to confer a significant predisposition to AP\u2010mediated kidney diseases. This review aims to explore how our current understanding will make it possible to identify the mechanisms that underlie AP\u2010mediated kidney diseases and to discuss the available clinical evidence that supports complement\u2010directed therapies. Although the value of limiting uncontrolled complement activation has long been recognized, incorporating complement\u2010targeted treatments into clinical use has proved challenging. Availability of anti\u2010complement therapy has dramatically transformed the outcome of atypical hemolytic uremic syndrome, one of the most severe kidney diseases. 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