title: ACE insertion/deletion polymorphism and diabetic nephropathy: clinical implications of genetic information.
abstract: 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.
authors.affiliation: Renal Division, Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Dogok-Dong, Gangnam-Gu, Seoul 146-92, Republic of Korea.
authors.forename: Sung-Kyu
authors.initials: SK
authors.lastname: Ha
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D003928:Diabetic Nephropathies / Q000188:drug therapy / Q000201:enzymology / Q000235:genetics*; D018450:Disease Progression; D020022:Genetic Predisposition to Disease; D006801:Humans; D007676:Kidney Failure, Chronic / Q000188:drug therapy / Q000201:enzymology / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010641:Phenotype; D011110:Polymorphism, Genetic; D011507:Proteinuria / Q000188:drug therapy / Q000201:enzymology / Q000235:genetics; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000235:genetics*; D012307:Risk Factors; D016896:Treatment Outcome
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A