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Recently it has become clear that, in addition to ischemia/reperfusion injury and posttransplant recipient-related factors, the induction of brain death would be a significant risk factor for posttransplant graft dysfunction. Brain death-related systemic changes and their effect on the hormonal and hemodynamic condition of the donor have been previously described. Now, an antigen-independent immunologic tissue activation in potential donor organs has been observed. In animal models this tissue activation is responsible for an increase of the immunogenicity of donor organs, such as liver and kidney, resulting in inferior function and decreased survival. The authors assume that cytoprotection and specific attempts to downregulate this immunogenicity will enhance graft function and have a beneficial effect in outcome after transplantation.

Original publication




Journal article


Current Opinion in Organ Transplantation

Publication Date





75 - 82