Background:

The arteriovenous fistula (AVF) is the first option as vascular access for patients with end-stage renal disease. The main cause of failure is stenosis of the venous portion of the AVF secondary to intimal hyperplasia.

Material and methods:

The objective of this study was to evaluate the relative expression of miR-145, miR-146, and miR-155. We used an experimental model of intimal hyperplasia creating an AVF. We included six Wistar Rats. The analysis and validation of miR-145, miR-146, and miR-155 was performed using real-time polymerase chain reaction.

Results:

There is a down-regulation of miR-145 in the vein (0.233 ± 0.3, p = 0.0030) and artery (0.33 ± 0.4, p = 0.0630), compared to the control. Likewise, we found upregulation of miR-146 in the vein (29 ± 0.25, p = 0.0256) and artery (34.66 ± 0.35, p = 0.0345) compared to the control and upregulation of miR-155 in the vein (20 ± 0.39, p = 0.0231) and artery (22.66 ± 0.49, p = 0.0234) compared to the control.

Conclusions:

We found alterations in the expression of miR-145, miR-146, and miR-155 comparing the fistula versus control, both in the arterial and venous portions in an experimental model of AVF.