Relationship between Monocytes and Stenosis-Related Autologous Arteriovenous Fistula Dysfunction.

BACKGROUND

Arteriovenous fistula (AVF) is considered to be the best choice of vascular access, but the maturation rate and patency rate of AVF are not satisfactory. Many studies have explored the influencing factors of AVF failure but do not involve the direct relationship between monocyte count and AVF failure. This study aims to explore the relationship between monocyte count and AVF dysfunction related to stenosis.

METHODS

From September 2017 to September 2018, basic clinical data and laboratory parameters of patients were collected. All included patients were followed up to September 2019. The stenosis-related AVF failure events that occurred after the patient included in the study and the time of their occurrence were recorded. All patients were divided into 3 groups based on the tertile of monocyte count. Kaplan-Meier method was used to compare the patency rate of AVF in each group. The effects of variables on AVF failure were analyzed. A multivariate Cox regression model with p < 0.05 was included in the univariate Cox regression analysis.

RESULTS

A total of 120 patients were included in this study. According to the recorded baseline monocyte count levels, they were divided into 3 groups according to their tertiles, 34 cases in the T1 group (T1 < 0.32 × 109/L), 44 cases in the T2 group (0.32 ≤ T2 < 0.51 × 109/L), and 42 cases in T3 group (T3 ≥0.51 × 109/L). After a median follow-up of 20 months, a total of 31 AVF failure events occurred. Kaplan-Meier survival curves showed that patients with a baseline monocyte count ≥0.51 × 109/L had the lowest patency rate of AVF (log-rank test χ2 = 7.525, p = 0.023). After adjusting to basic clinical data and biochemical indicators, there were statistically significant differences in patency rates of the 3 groups (hazard ratio = 2.774, 95% CI = 1.092-7.043).

CONCLUSION

Monocyte count ≥0.51 × 109/L is an independent risk factor for AVF failure, and AVF failure caused by monocytes may be driven by inflammation.