Arteriovenous fistula patency associated with angiotensin-converting enzyme I/D polymorphism and ACE inhibition or AT1 receptor blockade.
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.
Moon
Ju-Young
JY
Department of Internal Medicine, East West Neo Medical Center of Kyung Hee University, Kyung Hee University, Seoul, Korea.
Jeong
Kyung-Hwan
KH
Paik
Seung-Sook
SS
Han
Jae-Joon
JJ
Lee
Sang-Ho
SH
Lee
Tae-Won
TW
Ihm
Chun-Gyoo
CG
Kim
Myung-Jae
MJ
Chung
Joo-Ho
JH
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*
D000806:Angiotensin-Converting Enzyme Inhibitors; D044140:Receptor, Angiotensin, Type 1; D007703:Peptidyl-Dipeptidase A