Akman B, Tarhan C, Arat Z, Sezer S, Ozdemir F N
Department of Nephrology, Faculty of Medicine, Baskent University, Ankara, Turkey.
Ren Fail. 2009;31(3):196-200. doi: 10.1080/08860220802669826.
Aim. Renin-angiotensin system (RAS) gene mutations have been implicated as a risk factor for the presence and progression of renal disease in vesicoureteral reflux (VUR). However, the results are contradictory, and the effects of RAS polymorphisms in VUR patients with end-stage renal disease (ESRD) have not been defined yet. This study was designed to evaluate the angiotensin-converting enzyme insertion/deletion (ACE-I/D), angiotensinogen (AGT) M235T, and angiotensin II receptor type 1 (ATR1) A1166C and type 2 (ATR2) C3123A gene polymorphisms as risk factors for progression to ESRD in patients with VUR. Methods. ACE-I/D, AGT-M235T, ATR1-A1166C, and ATR2-C3123A were identified in 161 ESRD patients (52 female, 109 male; 77 renal transplant, 84 dialysis; age: 34.4 +/- 11.2 years). VUR was the ESRD etiology in 40 patients. Genetic polymorphisms of the ACE gene I/D, AGT gene M235T, ATR1 gene A1166C, and ATR2 gene C3123A were identified in all of the patients. Results. We detected no linkage between genetic polymorphisms of ATR1-, ATR2-, AGT-, and VUR-related ESRD. When ACE gene was considered, VUR(+) patients had 63.6% DD, 36.4% ID, and no II alleles, whereas VUR(-) patients had 48.6% DD, 43.2% ID, and 8.1% II alleles. Conclusion. A striking feature of VUR-related ESRD patients was the absence of II alleles, so the DD genotype may be accepted as a genetic susceptibility factor for progression to ESRD in VUR patients.
目的。肾素 - 血管紧张素系统（RAS）基因突变被认为是膀胱输尿管反流（VUR）患者肾脏疾病发生和进展的危险因素。然而，结果相互矛盾，且RAS基因多态性在终末期肾病（ESRD）的VUR患者中的作用尚未明确。本研究旨在评估血管紧张素转换酶插入/缺失（ACE - I/D）、血管紧张素原（AGT）M235T、血管紧张素II 1型受体（ATR1）A1166C和2型受体（ATR2）C3123A基因多态性作为VUR患者进展为ESRD的危险因素。方法。在161例ESRD患者（52例女性，109例男性；77例肾移植，84例透析；年龄：34.4±11.2岁）中鉴定ACE - I/D、AGT - M235T、ATR1 - A1166C和ATR2 - C3123A。40例患者的ESRD病因是VUR。在所有患者中鉴定ACE基因I/D、AGT基因M235T、ATR1基因A1166C和ATR2基因C3123A的基因多态性。结果。我们未检测到ATR1、ATR2、AGT和VUR相关的ESRD基因多态性之间的联系。当考虑ACE基因时，VUR（+）患者有63.6%的DD、36.4%的ID，无II等位基因，而VUR（ - ）患者有48.6%的DD、43.2%的ID和8.1%的II等位基因。结论。VUR相关的ESRD患者的一个显著特征是缺乏II等位基因，因此DD基因型可被视为VUR患者进展为ESRD的遗传易感性因素。
