Abstract
Purpose of ReviewOver the past two decades, significant strides made in our understanding of the etiology of antibody-mediated rejection (AMR) in transplantation have put the complement system in the spotlight. Here, we review recent progress made in the field of pharmacologic complement inhibition in clinical transplantation and aim to understand the impact of this therapeutic approach on outcomes in transplant recipients.Recent FindingsEncouraged by the success of agents targeting the complement cascade in disorders of unrestrained complement activation like paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS), investigators are testing the safety and efficacy of pharmacologic complement blockade in mitigating allograft injury in conditions ranging from AMR to recurrent post-transplant aHUS, C3 glomerulopathies and antiphospholipid anti-body syndrome (APS). A recent prospective study demonstrated the efficacy of terminal complement inhibition with eculizumab in the prevention of acute AMR in human leukocyte antigen (HLA)-incompatible living donor renal transplant recipients. C1 esterase inhibitor (C1-INH) was well tolerated in two recent studies in the treatment of AMR and was associated with improved renal allograft function.SummaryPharmacologic complement inhibition is emerging as valuable therapeutic tool, especially in the management of highly sensitized renal transplant recipients. Novel and promising agents that target various elements in the complement cascade are in development.Graphical ᅟ
Highlights
Improved understanding of the role of the immune system in allograft rejection, elucidation of the molecular mechanisms underlying graft failure and advances in immunosuppressive therapy have led to significant progress in the field of kidney transplantation in the last 50 years [1]
We provide an overview of the existing evidence supporting the use of pharmacologic complement inhibition as a therapeutic strategy in various settings in organ transplantation
Complement blockade may be a viable option for prevention of post-transplant recurrence in patients with atypical hemolytic uremic syndrome (aHUS) as evidenced by results documented in several pediatric case reports with demonstrable genetic abnormalities in the complement factor-H (CFH) gene [34, 36,37,38]
Summary
Summary Pharmacologic complement inhibition is emerging as valuable therapeutic tool, especially in the management of highly sensitized renal transplant recipients. Novel and promising agents that target various elements in the complement cascade are in development.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
