The complement cascade, traditionally considered an effector arm of innate immunity
required for host defense against pathogens, is now recognized as a crucial pathogenic
mediator of various kidney diseases. Complement components produced by the liver and
circulating in the plasma undergo activation through the classical and/or mannose-binding
lectin pathways to mediate anti-HLA antibody-initiated kidney transplant rejection and
autoantibody-initiated GN, the latter including membranous glomerulopathy, antiglomerular …