The importance of the
complement system in renal
ischemia-reperfusion injury and acute rejection is widely recognized, however its contribution to the pathogenesis of tissue damage in the donor remains underexposed.
Brain-dead (BD) organ donors are still the primary source of organs for
transplantation.
Brain death is characterized by hemodynamic changes, hormonal dysregulation, and immunological activation. Recently, the
complement system has been shown to be involved. In BD organ donors,
complement is activated systemically and locally and is an important mediator of
inflammation and graft injury. Furthermore, complement activation can be used as a
clinical marker for the prediction of graft function after
transplantation. Experimental models of BD have shown that inhibition of the
complement cascade is a successful method to reduce
inflammation and injury of donor grafts, thereby improving graft function and survival after
transplantation. Consequently,
complement-targeted
therapeutics in BD organ donors form a new opportunity to improve organ quality for
transplantation. Future studies should further elucidate the mechanism responsible for complement activation in BD organ donors.