ABSTRACT
INTRODUCTION: Growing experimental evidence suggests that the state of brain death (BD) activates surface molecules on peripheral organs by the massive release of macrophage- and T cell-associated cytokines as well as adhesion molecules into the circulation. The question is whether the sequelae of the BD process substantially influences the quality of the donor organ, the ensuing host response, or the ultimate transplant outcome. Our aim was to compare explosive BD with gradual-onset injury in terms of a trigger of the host immune mechanisms accelerating acute rejection processes. MATERIALS AND METHODS: This retrospective study included 149 cadaveric donors whose kidneys were transplanted in to 264 recipients. Exclusion criteria were previous transplants and hyperimmmunized patients. Donor variables were: sex, age, etiology of death, and hemodynamic conditions during the 24 hours prior to death. The recipient variables included, all possible conditions known to induce rejection. RESULTS: Cox analysis revealed the following factors to be predictive of acute vascular rejection: initial immunosuppression without induction (risk ratio [RR] 1.83; 95% confidence interval [CI] 1.02 to 3.25; P = .039) which there was a trend to an impact of a regimen without tacrolimus (RR 1.84; 95% CI 0.85 to 3.98; P = .099), or of recipient age < 30 years (RR 2.17; 95% CI 1.06 to 4.48); P = .053) or lower mean donor blood pressure during the 3 hours prior to death (RR 1.17; 95% CI 1.00 to 1.37; P = .054). CONCLUSIONS: Greater sympathetic activity during brain death produces nonspecific endothelial damage and increases organ immunogenicity, promoting rejection.
