Yildiz Alaattin, Yazici Halil, Cine Naci, Akkaya Vakur, Kayacan S Mehmet, Sever Mehmet Sükrü, Erginel-Unaltuna Nihan
Department of Internal Medicine, Istanbul University, Istanbul School of Medicine, Turkey.
Clin Transplant. 2002 Jun;16(3):173-9. doi: 10.1034/j.1399-0012.2002.01058.x.
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.
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.
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.
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.
慢性移植肾失功（CAD）是肾移植失败的主要原因，可能由免疫和非免疫血流动力学因素引起。肾素 - 血管紧张素系统与肾小球内高血压的发生有关，在慢性肾病进展中起核心作用。据报道，ACE基因第16内含子的多态性可预测循环血管紧张素II水平。本研究旨在探讨受者和供者血管紧张素转换酶（ACE）基因型对肾移植受者CAD发生的影响。
共纳入143例肾移植受者（男95例，女48例，平均年龄32±10岁）。为排除冷缺血的影响，仅选择活体供者移植的患者。分析CAD发生相关的因素包括供者和受者年龄、急性排斥反应病史、高血压和高胆固醇血症的存在、血清尿酸水平及ACE基因多态性。
40例患者（28%）发生CAD。59例肾移植受者（42%）及其31例供者（37%）检测到纯合缺失型ACE基因多态性。比较发生CAD和未发生CAD的患者，CAD（+）组的供者年龄、急性排斥反应发生率、高血压和血清尿酸水平显著更高。受者和供者的ACE基因型均与发生CAD的时间无关。Cox回归分析显示供者年龄（p < 0.001）、高血压的存在（p = 0.002）和血清尿酸水平（p = 0.009）是预测CAD发生的独立因素，但供者和受者的ACE基因型均不是。
供者年龄、高血压的存在和血清尿酸水平是独立因素。供者和受者的ACE基因型似乎对活体供者移植患者CAD的发生没有影响。
