Outcomes of deceased-donor kidney transplants are worse than outcomes of living donor transplants, a finding partially attributed to inflammation resulting from worse ischemia-reperfusion injury of the kidney. Preclinical studies by the Tilney lab remarkably demonstrated that donor brain death (DBD) induced marked increases in proinflammatory gene expression in donor organs pre-transplant. Subsequent work verified that brain death in donors associated with increased the levels of multiple proinflammatory cytokines (including tumor necrosis factor alpha, interleukin-6, (1) 1. Murugan, R. ∙ Venkataraman, R. ∙ Wahed, A.S. ... Increased plasma interleukin-6 in donors is associated with lower recipient hospital-free survival after cadaveric organ transplantation Crit Care Med. 2008; 36 (6):1810-1816 Google Scholar ) and complement products (C5a), and small studies suggested these elevations associate with worse outcomes. However, large studies relating donor inflammation to posttransplant outcomes, and testing whether these associations apply to kidneys from donation after cardiac death (DCD) have not been reported.
Qian et al. (Sun,) studied this question.