ACE Insertion/Deletion Polymorphism and Diabetic Nephropathy: Clinical Implications of Genetic Information

Approximately 20–40% of diabetic patients develop nephropathy which is the leading cause of ESRD in developed countries. The ACE I/D polymorphism is thought to be a marker for functional polymorphism which regulates circulating and tissue ACE activity. While the initial study found a protective effe...

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Main Author: Sung-Kyu Ha
Format: Article
Language:English
Published: Hindawi Limited 2014-01-01
Series:Journal of Diabetes Research
Online Access:http://dx.doi.org/10.1155/2014/846068
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spelling doaj-21ed63936697407499361732467889bd2020-11-24T23:04:19ZengHindawi LimitedJournal of Diabetes Research2314-67452314-67532014-01-01201410.1155/2014/846068846068ACE Insertion/Deletion Polymorphism and Diabetic Nephropathy: Clinical Implications of Genetic InformationSung-Kyu Ha0Renal Division, Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Dogok-Dong, Gangnam-Gu, Seoul 146-92, Republic of KoreaApproximately 20–40% of diabetic patients develop nephropathy which is the leading cause of ESRD in developed countries. The ACE I/D polymorphism is thought to be a marker for functional polymorphism which regulates circulating and tissue ACE activity. While the initial study found a protective effect of the II genotype on the development of nephropathy in IDDM patients, subsequent studies have addressed the role of ACE I/D polymorphism in the development and progression of diabetic nephropathy. RAAS blockers are the first line drugs for the treatment hypertension associated with diabetes and have been widely used in everyday clinical practice for the purpose of reducing proteinuria in patients with various renal diseases. However, the antiproteinuric effect of RAAS blockers is variable and the percentage of reducing proteinuria is in the range of 20–80%. The antiproteinuric effect of RAAS blockers may be related to a number of factors: the type or the dose of RAAS blockers, the duration of therapy, the level of sodium intake, and the type of patient’s ACE I/D genotype. Besides the nongenetic factors, drug responses, can be influenced by ACE gene polymorphism. In this review, we discuss the relationship between ACE I/D polymorphism and diabetic nephropathy and therapeutic response of RAAS blockers.http://dx.doi.org/10.1155/2014/846068
collection DOAJ
language English
format Article
sources DOAJ
author Sung-Kyu Ha
spellingShingle Sung-Kyu Ha
ACE Insertion/Deletion Polymorphism and Diabetic Nephropathy: Clinical Implications of Genetic Information
Journal of Diabetes Research
author_facet Sung-Kyu Ha
author_sort Sung-Kyu Ha
title ACE Insertion/Deletion Polymorphism and Diabetic Nephropathy: Clinical Implications of Genetic Information
title_short ACE Insertion/Deletion Polymorphism and Diabetic Nephropathy: Clinical Implications of Genetic Information
title_full ACE Insertion/Deletion Polymorphism and Diabetic Nephropathy: Clinical Implications of Genetic Information
title_fullStr ACE Insertion/Deletion Polymorphism and Diabetic Nephropathy: Clinical Implications of Genetic Information
title_full_unstemmed ACE Insertion/Deletion Polymorphism and Diabetic Nephropathy: Clinical Implications of Genetic Information
title_sort ace insertion/deletion polymorphism and diabetic nephropathy: clinical implications of genetic information
publisher Hindawi Limited
series Journal of Diabetes Research
issn 2314-6745
2314-6753
publishDate 2014-01-01
description Approximately 20–40% of diabetic patients develop nephropathy which is the leading cause of ESRD in developed countries. The ACE I/D polymorphism is thought to be a marker for functional polymorphism which regulates circulating and tissue ACE activity. While the initial study found a protective effect of the II genotype on the development of nephropathy in IDDM patients, subsequent studies have addressed the role of ACE I/D polymorphism in the development and progression of diabetic nephropathy. RAAS blockers are the first line drugs for the treatment hypertension associated with diabetes and have been widely used in everyday clinical practice for the purpose of reducing proteinuria in patients with various renal diseases. However, the antiproteinuric effect of RAAS blockers is variable and the percentage of reducing proteinuria is in the range of 20–80%. The antiproteinuric effect of RAAS blockers may be related to a number of factors: the type or the dose of RAAS blockers, the duration of therapy, the level of sodium intake, and the type of patient’s ACE I/D genotype. Besides the nongenetic factors, drug responses, can be influenced by ACE gene polymorphism. In this review, we discuss the relationship between ACE I/D polymorphism and diabetic nephropathy and therapeutic response of RAAS blockers.
url http://dx.doi.org/10.1155/2014/846068
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