Abstract:

Complement is an important component of innate immunity, as well as a bridge to regulate adaptive immunity. It is an important substance that mediates cellular inflammatory response and induces apoptosis. The cascade of the complement response is stictly regulated by the stringent control of the complennent regulatory proteins. Should the complement overactivated or regulate abnormally, it can cause damage to the host cells. In the glomerular microenvironment, dysregulation of the complement system can lead to C3 glomerulopathy and atypical hemolytic uremic syndrome. In addition, complement is also hyperactivated in many other inflammatory kidney diseases, such as ANCA-associated glomerulonephritis, lupus nephritis, IgA nephropathy, membranous nephropathy, and diabetic nephropathy. In addition, it may mediate renal allograft injury by playing a role in ischemia-reperfusion injury and rejection. This article reviews the role of complement in the pathogenesis of glomerular diseases and related targeted therapy.

Key words: complement, kidney disease, targeted Therapy