Johns Hopkins University School of Medicine, Baltimore, MD, USA
The activation of the complement cascade pathway plays a pivotal role in the pathogenesis of the kidney allograft in several disorders.
Antibody mediated rejection (AMR) due to HLA, ABO or other antibodies has emerged as a major cause of allograft failure in recent years. Classic complement pathway activation that leads to the membrane attack complex formation is a major contributor to the tissue injury that occurs in AMR.
Alternative complement pathway activation is also a major cause of allograft dysfunction and failure in some disorders that affect the kidney transplant. Atypical hemolytic uremic syndrome (aHUS) and membranoproliferative glomerulonephritis (MPGN), in particular C3 Glomerulopathy, recur very commonly in the kidney allograft and may lead to allograft failure prematurely. Mutations of some alternative complements are the major causes of these diseases, which lead to early recurrence of these disorders in the transplanted kidney.
Anti C5-complemnet antibody has been used in the kidney transplant filed as a prophylactic and treatment of these complement mediated disorders with great success.
In here, we will present our center’s experience in utilizing anti-complements’ therapy in AMR, aHUS and MPGN disorders in kidney transplant patients.