Hemodynamic and Biologic Determinates of Arteriovenous Fistula Outcomes in Renal Failure Patients

Abstract

The outcome of patients with end-stage renal disease on hemodialysis depends on a functioning vascular access. Although a variety of access options are available, the arteriovenous fistula remains the best vascular access. Unfortunately the success rate of mature fistula use remains poor. The creation of an arteriovenous fistula is followed by altered hemodynamic and biological changes that may result in neointimal hyperplasia and eventual venous stenosis. This review provides an overview of these changes and the needed research to provide a long lasting vascular access and hence improve outcomes for patients with end-stage renal disease.

Reduction in anastomotic flow disturbance within a modified end‐to‐side arteriovenous fistula configuration: Results of a computational flow dynamic model

“…[14][15][16] As arterial and AVF flow increase significantly following surgery, physiological remodelling results in blood vessel dilatation to achieve normalization of those elevated WSS. 17,18 Disturbed flows in a newly created AVF are likely to have a direct impact on that ensuing vascular remodelling process with successful maturation more likely if flow disturbance is minimized. [19][20][21] There are some modifications required to surgical technique to create this configuration of AVF.…”

A randomized trial of vonapanitase (PATENCY-1) to promote radiocephalic fistula patency and use for hemodialysis

“…This increase in flow leads to vascular remodeling with dilation and medial thickening. 15,16 In this manner, the fistula matures and can be cannulated for hemodialysis. Unfortunately, many fistulas fail to mature successfully because of impaired outward vascular remodeling.…”

Contribution of monoamine oxidases to vascular oxidative stress in patients with end-stage renal disease requiring hemodialysis

“…Therefore, understanding the complex pathophysiology that underlies endothelial dysfunction in the setting of renal failure is crucial for a long-term viability of the vascular access. In particular, the hemodynamic abnormalities elicited by the surgical anastomosis of a high pressure artery to a low pressure vein have been systematically studied (Hammes 2015); indeed, neointimal hyperplasia and subsequent venous stenosis have been reported to be the major culprits responsible for the vascular access failure (Stolic 2013).…”

“…Clearly, chronic accumulation of uremic toxins is primarily responsible for increased arterial stiffness, endothelial hyperplasia and calcification in patients with renal failure (Nemcsik et al 2012). Moreover, hemodialysis is a treatment that contributes per se to the oxidative stress (and reduced NO formation) through the shear stress of the venous endothelial cells (Hammes 2015).…”