The deletion polymorphism of the ACE gene is not an independent risk factor for renal scarring in children with vesico-ureteric reflux

被引:13
|
作者
Dudley, J
Johnston, A
Gardner, A
McGraw, M
机构
[1] Southmead Gen Hosp, Dept Paediat Nephrol, Bristol BS10 5NB, Avon, England
[2] Southmead Gen Hosp, Dept Cytogenet, Bristol BS10 5NB, Avon, England
关键词
ACE gene polymorphisms; renal scarring; vesico-ureteric reflux;
D O I
10.1093/ndt/17.4.652
中图分类号
R3 [基础医学]; R4 [临床医学];
学科分类号
1001 ; 1002 ; 100602 ;
摘要
Background. The deletion (D) polymorphism of the gene encoding angiotensin-I converting enzyme has been implicated as a risk factor for progressive renal disease in several conditions. This study was designed to evaluate the association between homozygosity for the D allele and susceptibility to renal scarring in children with vesico-ureteric reflux (VUR). Methods. Two-hundred-and-six children with VUR (all grades) were recruited into the study. Patients were stratified into two groups according to the presence or absence of renal scarring. One-hundred-and-twelve patients (group 1) had evidence of renal scarring. Ninety-four children had no evidence of renal scarring (group 2). ACE genotypes were determined by polymerase chain reaction (PCR) amplification of genomic DNA samples. Results. There was no association between the DD polymorphism and the presence of renal scarring. Genotype frequencies in group 1 were: II, 29, ID, 56, and DD, 27; and in group 2 were: II, 12; ID, 52, DD, 30 (P = 0.21). Neither was there evidence supporting a 'dominant' D allele. There was no association between the DD genotype and the presence of proteinuria or reduced renal function (P > 0.05). Hypertension was seen more frequently in those individuals with the DD genotype, compared with the other two genotypes (P = 0.012). Conclusion. We cannot confirm previous reports that children with vesico-ureteric reflux who are homozygous for the deletion polymorphism of the ACE gene are more susceptible to renal scarring than heterozygotes and II homozygotes.
引用
收藏
页码:652 / 654
页数:3
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