Brain death of the donor is an important risk factor influencing graft outcome. In addition to its nonspecific effects, it potentiates graft immunogenicity and increases host alloresponsiveness. Thus brain death in addition to other unspecific injuries such as organ procurement, preservation and consequences of ischemia/reperfusion injury, contributes towards the change of an inert organ to an immunological altered graft. Prior to engraftment, brain death initiates a cascade of molecular and cellular events including the release of proinflammatory mediators leading to cellular infiltrates. Those events may affect the incidence of both acute and chronic changes, developing and contributing to reduced graft survival. Consequently, strategies to reduce the immunogenicity or the pro-inflammatory status of the graft are becoming more attractive and might even help to improve organ quality and graft function.
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