Is AV fistula patency associated with angiotensin-converting enzyme (ACE) polymorphism and ACE inhibitor intake?

Hemodialysis treatment requires a well-functioning vascular access. Access patency is limited by the development of venous intimal hyperplasia, which predisposes to fistula stenosis and subsequent thrombosis. In animal models, the renin-angiotensin system has a major role in the development of intimal hyperplasia. We investigated the association of the insertion/deletion polymorphism of the angiotensin-converting enzyme (ACE) and arteriovenous fistula patency in hemodialysis patients.

In a longitudinal study, 137 hemodialysis patients who had undergone creation of a primary AV fistula were genotyped. The main study endpoint was unassisted access patency (time from fistula placement to the first episode of access failure). In addition, the intake of drugs blocking the renin-angiotensin system was assessed.

Fistula patency 12 months after fistula creation was 72% (DD patients), 65% (ID patients), and 73% (II patients; p = 0.40). Long-term intake of ACE inhibitors or AT-1 antagonists failed to increase fistula patency (p = 0.33).

We suggest that pharmacological inhibition of the renin-angiotensin system is of limited value for prevention of arteriovenous fistula stenosis. Alternative strategies to prolong fistula patency should be studied.