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Abstract
The complement cascade is part of the innate immune system whose actions protect hosts from pathogens. Recent research shows complement involvement in a wide spectrum of renal disease pathogenesis including antibody-related glomerulopathies and non-antibody-mediated kidney diseases, such as C3 glomerular disease, atypical hemolytic uremic syndrome, and focal segmental glomerulosclerosis. A pivotal role in renal pathogenesis makes targeting complement activation an attractive therapeutic strategy. Over the last decade, a growing number of anti-complement agents have been developed; some are approved for clinical use and many others are in the pipeline. Herein, we review the pathways of complement activation and regulation, illustrate its role instigating or amplifying glomerular injury, and discuss the most promising novel complement-targeting therapies.
Highlights
Complement CascadeThe complement system consists of soluble or membrane-bound molecules, mostly zymogens, activated through a tightly regulated proteolytic cascade [1,2]
The complement cascade is part of the innate immune system whose actions protect hosts from pathogens
CFHR1, CFHR3, and CFHR5 especially have been studied for their role in IgA nephropathy (IgAN) [29,31]; another study of 1126 Chinese patients concluded that circulating CFHR5 levels are an independent risk factor for the disease: levels were higher in IgAN subjects compared to heathy controls, and correlated directly with worst Oxford MEST pathology score, a lower glomerular filtration rate (GFR), and hypertension [32]
Summary
The complement system consists of soluble or membrane-bound molecules, mostly zymogens, activated through a tightly regulated proteolytic cascade [1,2]. Current understanding of complement immune mechanisms include (1) functioning as opsonins; (2) producing chemoattractants to recruit immune cells thereby enhancing site specific angiogenesis, vasodilation and coagulation cascade regulator; and (3) functioning as an enhancing bridge to adaptive T and B lymphocyte responses [3]. Current research suggests that abnormal complement activation plays a role in autoimmune inflammatory diseases and in those targeting the kidney
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