title: Arteriovenous fistula patency associated with angiotensin-converting enzyme I/D polymorphism and ACE inhibition or AT1 receptor blockade.
abstract: BACKGROUND
  Compromise of arteriovenous fistula (AVF) patency is caused by venous intimal hyperplasia. Many studies indicated that the renin-angiotensin-aldosterone system plays an important role in the development of intimal hyperplasia. Here we determined whether angiotensin-converting enzyme (ACE) I/D polymorphism is an independent prognostic factor for AVF patency in hemodialysis (HD) patients.
  
  
  METHODS
  One hundred and fifty-five HD patients with native AVF were enrolled and genotyped, retrospectively. The primary end point was unassisted patency of the AVF, which was defined as the time from the first fistula surgery to the AVF failure.
  
  
  RESULTS
  The unassisted AVF patency at 58 months was 47.0% in the DD genotype group and 71.8/82.9% in ID/II groups (p < 0.01). ACE inhibitors (ACEI) or angiotensin II receptor blockers (ARB) intake had significant impact on AVF patency in the ACE DD group (p = 0.03). Using a Cox-adjusted model, we observed a significant correlation between the increase in the incidence of AVF failure and diabetic nephropathy, higher mean serum phosphorus level, and the ACE DD genotype.
  
  
  CONCLUSIONS
  The ACE I/D polymorphism was associated with the development of AVF failure, and a preventive role of ACEI or ARB intake on AVF patency in ACE DD patients was observed.
authors.affiliation: Department of Internal Medicine, East West Neo Medical Center of Kyung Hee University, Kyung Hee University, Seoul, Korea.
authors.forename: Ju-Young
authors.initials: JY
authors.lastname: Moon
authors.forename: Kyung-Hwan
authors.initials: KH
authors.lastname: Jeong
authors.forename: Seung-Sook
authors.initials: SS
authors.lastname: Paik
authors.forename: Jae-Joon
authors.initials: JJ
authors.lastname: Han
authors.forename: Sang-Ho
authors.initials: SH
authors.lastname: Lee
authors.forename: Tae-Won
authors.initials: TW
authors.lastname: Lee
authors.forename: Chun-Gyoo
authors.initials: CG
authors.lastname: Ihm
authors.forename: Myung-Jae
authors.initials: MJ
authors.lastname: Kim
authors.forename: Joo-Ho
authors.initials: JH
authors.lastname: Chung
mesh_terms: D000328:Adult; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D001166:Arteriovenous Shunt, Surgical / Q000639:trends*; D005260:Female; D005500:Follow-Up Studies; D017353:Gene Deletion; D006801:Humans; D007676:Kidney Failure, Chronic / Q000235:genetics / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D016254:Mutagenesis, Insertional / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D044140:Receptor, Angiotensin, Type 1 / Q000502:physiology*; D014654:Vascular Patency / Q000502:physiology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D044140:Receptor, Angiotensin, Type 1; D007703:Peptidyl-Dipeptidase A