Investigation of association between donors' and recipients' NADPH oxidase p22phox C242T polymorphism and acute rejection, delayed graft function and blood pressure in renal allograft recipients

BackgroundProduction of reactive oxygen species (ROS) and thereby induction of oxidative stress seem to be one of the major mediators of inflammatory adverse outcomes after renal transplantation. p22phox is a polymorphic subunit of NAD(P)H-oxidase that is critical for activation and stabilization of the enzyme. This enzyme is involved in the production of superoxide that triggers inflammatory injuries to the kidney. So in this study, the association between donors and recipients' C242T polymorphism of p22phox and acute rejection (AR), delayed graft function (DGF), creatinine clearance (CrCl), and blood pressure in renal-allograft recipients was studied.MethodsOne hundred ninety six donor–recipient pairs were studied. The C242T polymorphism of p22phox was determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). According to p22 genotype, the subjects were divided in wild-type (CC) and T allele carriers (CT + TT). Transplantation outcomes were determined using acute rejection and delayed graft function criteria. The mean arterial pressure was also measured monthly after transplantation.ResultsThere was a significant association between the recipients' p22phox polymorphism and DGF occurrence (OR = 2.5, CI: 1.2–4.9, p = 0.0009). No significant association was detected between donors' p22phox polymorphism and AR and DGF events. CrCl during the six months follow-up after transplantation was lower in the patients who received allograft from donors carrying 242T allele (B = − 12.8, CI: − 22.9–12.8 (− 22.9 to − 2.6)). Changes in the blood pressure were not different among the patients having different genotypes of p22phox.ConclusionThese results suggest that the recipients' p22phox C242T polymorphism may be a major risk factor for DGF in renal transplantation. Moreover, the donors' 242T allele seems to affect the rate of CrCl in the renal allograft recipients.