Variance of ACE and AT1 receptor gene does not influence the risk of neonatal acute renal failure

被引:16
作者
Nobilis, A
Kocsis, I
Tóth-Heyn, P
Treszl, A
Schuler, A
Tulassay, T
Vásárhelyi, B
机构
[1] Semmelweis Univ, Dept Pediat 1, H-1083 Budapest, Hungary
[2] Semmelweis Univ, Dept Obstet & Gynecol 2, H-1083 Budapest, Hungary
[3] Semmelweis Univ, Joint Res Program Dept Pediat 1 & Hungarian Acad, H-1083 Budapest, Hungary
[4] Budai Childrens Hosp, PKU Lab, Budapest, Hungary
关键词
acute renal failure; very low birth weight infant; angiotensin converting enzyme; angiotensin II; type; 1; receptor; genetic polymorphism;
D O I
10.1007/s004670100028
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
High neonatal activity of the renin-angiotensin system (RAS) is crucial for the maintenance of glomerular filtration of the newborn. The aim of the present study was to investigate whether genetic polymorphisms leading to lower angiotensin converting enzyme activity (ACE) or impaired functionality of angiotensin 11 (All) type 1 receptor (AT1R) might predispose very low birth weight newborns (VLBWs) to the development of acute renal failure (ARF). The medical records of 110 VLBW infants were analyzed. ARF developed in 42 of them during the first postnatal week, while 68 neonates exhibited normal renal function. The ACE I/D polymorphism and the A(1166)C variants of AT1R were determined from dried blood samples. The frequency of the ACE I allele did not differ in ARF and non-ARF groups (0.307 and 0.284); the frequency of the AT1R C-1166 variant was also the same in ARF and non-ARF groups (0.250 and 0.227). Although low activity of RAS has been implicated in the development of neonatal ARF and data indicated that the functionality of RAS is influenced by the I/D variants of the ACE gene and the A(1166)C variant of the AT1R gene, we could not demonstrate any effect of these polymorphisms on the development of ARF in VLBW infants.
引用
收藏
页码:1063 / 1066
页数:4
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