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ACE insertion/deletion polymorphism and diabetic nephropathy: clinical implications of genetic information

DC Field Value Language
dc.contributor.author하성규-
dc.date.accessioned2015-12-28T10:58:56Z-
dc.date.available2015-12-28T10:58:56Z-
dc.date.issued2014-
dc.identifier.issn2314-6745-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/138440-
dc.description.abstractApproximately 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.-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.relation.isPartOfJOURNAL OF DIABETES RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAngiotensin II Type 1 Receptor Blockers/therapeutic use-
dc.subject.MESHAngiotensin-Converting Enzyme Inhibitors/therapeutic use-
dc.subject.MESHAnimals-
dc.subject.MESHDiabetic Nephropathies/drug therapy-
dc.subject.MESHDiabetic Nephropathies/enzymology-
dc.subject.MESHDiabetic Nephropathies/genetics*-
dc.subject.MESHDisease Progression-
dc.subject.MESHGenetic Predisposition to Disease-
dc.subject.MESHHumans-
dc.subject.MESHKidney Failure, Chronic/drug therapy-
dc.subject.MESHKidney Failure, Chronic/enzymology-
dc.subject.MESHKidney Failure, Chronic/genetics*-
dc.subject.MESHPeptidyl-Dipeptidase A/genetics*-
dc.subject.MESHPhenotype-
dc.subject.MESHPolymorphism, Genetic*-
dc.subject.MESHProteinuria/drug therapy-
dc.subject.MESHProteinuria/enzymology-
dc.subject.MESHProteinuria/genetics-
dc.subject.MESHRenin-Angiotensin System/drug effects-
dc.subject.MESHRenin-Angiotensin System/genetics*-
dc.subject.MESHRisk Factors-
dc.subject.MESHTreatment Outcome-
dc.titleACE insertion/deletion polymorphism and diabetic nephropathy: clinical implications of genetic information-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorSung Kyu Ha-
dc.identifier.doi10.1155/2014/846068-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA04252-
dc.relation.journalcodeJ01378-
dc.identifier.eissn2314-6753-
dc.identifier.pmid25587546-
dc.contributor.alternativeNameHa, Sung Kyu-
dc.contributor.affiliatedAuthorHa, Sung Kyu-
dc.citation.volume2014-
dc.citation.startPage846068-
dc.identifier.bibliographicCitationJOURNAL OF DIABETES RESEARCH, Vol.2014 : 846068, 2014-
dc.identifier.rimsid49173-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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