Association of the ACE gene polymorphism with the progression of autosomal dominant polycystic kidney disease.
10.3346/jkms.2000.15.4.431
- Author:
Kyu Beck LEE
1
;
Un Kyung KIM
;
Chung Choo LEE
Author Information
1. Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea. kyubeck+AEA-samsung.co.kr
- Publication Type:Original Article ; Comparative Study ; Research Support, Non-U.S. Gov't
- Keywords:
Kidney, Polycystic, Autosomal Dominant;
Peptidyl Dipeptidase A;
Polymorphism(Genetics);
Kidney Failure;
Hypertension
- MeSH:
Adult;
Aged;
Comparative Study;
Disease Progression;
Female;
Genetic Predisposition to Disease;
Genotype;
Human;
Hypertension, Renal/etiology;
Hypertension, Renal/epidemiology;
Kidney Failure, Chronic/etiology;
Kidney Failure, Chronic/epidemiology;
Korea/epidemiology;
Male;
Middle Age;
Peptidyl-Dipeptidase A/genetics+ACo-;
Polycystic Kidney, Autosomal Dominant/genetics+ACo-;
Polycystic Kidney, Autosomal Dominant/epidemiology;
Polycystic Kidney, Autosomal Dominant/enzymology;
Polycystic Kidney, Autosomal Dominant/complications;
Polymerase Chain Reaction;
Polymorphism (Genetics)+ACo-;
Prevalence
- From:Journal of Korean Medical Science
2000;15(4):431-435
- CountryRepublic of Korea
- Language:English
-
Abstract:
Renin-angiotensin system is considered important in the genesis of hypertension and development of end-stage renal disease (ESRD) in autosomal dominant polycystic kidney disease (ADPKD). The angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism has been associated with susceptibility to the development of some renal diseases. We investigated the association of ACE gene polymorphism with the progression to hypertension and ESRD in 108 patients with ADPKD. The ACE I/D polymorphism was amplified with the flanking primers by polymerase chain reaction. In patients genotyped for ACE gene polymorphism, the frequencies of DD (15+ACU-), ID (51+ACU-) and II (34+ACU-) genotypes were similar to those of the general population. Of the 108 patients, 64 (59+ACU-) developed hypertension and 24 (22+ACU-) reached ESRD at the time of study. The prevalence of hypertension was not significantly different among the three genotypes. The mean renal survival time was 53-6 yr in II genotype, 5510 yr in ID genotype and 529 yr in DD genotype which was not significantly different among them. Cumulative renal survival was not significantly different either. There was no association of ACE gene polymorphism with the prevalence of hypertension and renal survival in ADPKD. We suggest that ACE I/D polymorphism is not an important modifying gene in the progression of ADPKD.
