The effect of angiotensin converting enzyme gene polymorphism on chronic allograft dysfunction in living donor renal transplant recipients.
BACKGROUND
Chronic allograft dysfunction (CAD), the major cause of the failure of kidney allografts, may be caused by immunological and non-immunological haemodynamic factors. Renin-angiotensin system has been implicated in the development of intraglomerular hypertension and has a central role on progression in chronic renal disease. Polymorphism in 16th intron of the ACE gene has been reported to predict the circulating angiotensin II levels. The aim of this study was to investigate the effect of the both recipient and donor angiotensin converting enzyme (ACE) genotype on the development of CAD in renal allograft recipients.


METHODS
A total of 143 renal transplant recipients (95 male, 48 female, mean age 32 +/- 10 yr) were included. In order to exclude the effect of cold ischaemia, only patients transplanted from living donors were selected. Factors analysed in the development of CAD were donor and recipient age, past history of acute rejection, presence of hypertension and hypercholesterolaemia, serum uric acid level and ACE gene polymorphism.


RESULTS
Forty of the patients (28%) had CAD. Homozygous deletion type ACE gene polymorphism was detected in 59 renal transplant recipients (42%) and in 31 donors of the patients (37%). On comparing patients with and without CAD, donor age, rate of acute rejection and hypertension and serum uric acid levels were significantly higher in CAD (+) groups. Neither recipient nor donor ACE genotype was associated with time to CAD. Cox regression analysis revealed donor age (p < 0.001), presence of hypertension (p=0.002) and serum uric acid levels (p=0.009), but neither donor nor recipient ACE genotype as independent factors for predicting development of CAD.


CONCLUSIONS
Donor age, presence of hypertension and serum uric acid levels was independent factors. Donor and recipient ACE genotype seemed to have no influence on the development of CAD in living donor transplanted patients.
Yildiz
Alaattin
A
Department of Internal Medicine, Istanbul University, Istanbul School of Medicine, Turkey. alaattiny@hotmail.com
Yazici
Halil
H
Cine
Naci
N
Akkaya
Vakur
V
Kayacan
S Mehmet
SM
Sever
Mehmet Sükrü
MS
Erginel-Unaltuna
Nihan
N
D000328:Adult; D002908:Chronic Disease; D005260:Female; D005838:Genotype; D006084:Graft Rejection / Q000235:genetics* / Q000276:immunology; D006801:Humans; D016030:Kidney Transplantation / Q000276:immunology* / Q000379:methods; D019520:Living Donors; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D012084:Renin-Angiotensin System / Q000235:genetics / Q000276:immunology; D014184:Transplantation, Homologous
D007703:Peptidyl-Dipeptidase A