Abstract
Donor brain death, cold preservation, and subsequent ischemia-reperfusion injury all participate in the pathology of primary graft dysfunction (PGD) and trigger immune responses. Our experimental studies suggest that this early immune response may initiate proinflammatory and profibrotic processes and develop into chronic rejection. In this clinical study, we investigated the role of proinflammatory cytokines as biomarkers for PGD.
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