2 Donor Acetaldehyde Dehydrogenase Gene Polymorphism Of Ring Spore, A Cause Of Acute Graft Function Damage And The Influence Of Graft Survival

ObjectiveThrough clinical and basic experiments to investigate the relation-ship between the activity of the transplanted kidney with impaired renal function and renal allograft survival and the Aldehyde dehydrogenase2(ALDH2), hope to determine the key elements of acute renal allograft dysfunction caused by cyclosporine A, and to provide new ideas for the prevention and treatment cyclosporine A (CsA) toxicity of acute renal injury.MethodsDetect the polymorphism of ALDH2by PCR-RFLP;analysis the impact of the ALDH2gene polymorphisms on renal graft function and survival combined with clinical data and follow-up; suppression and improve the ALDH2activity in animal experiments in mice by using Daidzin and Alda-l,to detect the impact of the ALDH2activity on the toxicity of CsA.ResultsIn clinical trials, there are two acute CsA toxicity cases in kidney transplant recipients whose ALDH2is wild-type, there are seven acute CsA toxicity cases in kidney transplant recipients whose donor is ALDH2mutant. The statistical analysis shows, that compared the kidney transplant recipients whose donor is ALDH2wild-type with the kidney transplant recipients whose donor is ALDH2mutant,the incidence of acute CsA poisoning is significant difference (P<0.05),there was statistically significant.In animal studies, the inhibition of ALDH2enzyme activity, makes the mouse renal tubular epithelial cell degeneration and necrosis severity; improving the activity of ALDH2enzyme, can reduce the renal tubular epithelial cell degeneration and necrosis extent.Conclusions1The impact on acute CsA nephrotoxicity injury in renal transp-lantation receptor of the donor ALDH2gene polymorphism exist: wild-type ALDH2receptors in acute CsA nephrotoxicity have protect-tive effect, the mutant ALDH2receptors in acute CsA nephrotoxicity do not have protective effect.2Improving the activity of ALDH2enzyme in tubular mitochondrial vivo in mice can reduce acute CsA nephrotoxicity of renal tubular epithelial cells;The inhibition of ALDH2activity, increases the acute CsA nephrotoxicity of renal tubular epithelial cells.