Retrospective analysis of statin use and arteriovenous fistula thrombosis in hemodialysis: Is there a dose-dependent effect?

Arteriovenous fistula (AVF) thrombosis is a major vascular access complication in hemodialysis (HD) patients, contributing to increased morbidity. Statins, known for their pleiotropic effects, may reduce AVF thrombosis risk, but evidence on dose-dependent effects is limited. This study evaluated the association between statin use, dose intensity, and AVF thrombosis in HD patients. Methods. A multicenter, retrospective cohort study was conducted using data from 562 HD patients with native AVFs across 10 dialysis clinics (May 2021–April 2025). Patients were categorized by statin use (users vs. non-users) and dose intensity (moderate vs. high vs. none). The primary outcome was AVF thrombosis; death was treated as a competing event. Kaplan-Meier survival curves and Fine and Gray subdistribution hazard models, adjusted for age, diabetes, dialysis vintage, Kt/V, glucose, calcium, blood flow, and pre-HD cardiovascular disease, were used to assess thrombosis risk. Results. Of 562 patients (median follow-up 59 months), 212 (37.7%) were statin users. AVF thrombosis occurred in 54 (9.6%) patients, with 11 (7.1%) in statin users vs. 43 (10.6%) in non-users (p = 0.006). Kaplan-Meier analysis showed lower thrombosis probability in statin users (log-rank p = 0.001), with high-intensity users having the lowest risk (p = 0.004). In the unadjusted Fine and Gray model, high-intensity statins were associated with reduced thrombosis risk (sHR 0.61, 95% CI 0.59–0.97, p = 0.03), with a significant dose-dependent trend (p = 0.018). The adjusted model showed no significant association (moderate: sHR 0.67, p = 0.16; high: sHR 0.57, p = 0.26). Conclusions. Statin use, particularly high-intensity, may reduce AVF thrombosis risk in HD patients, with a dose-dependent trend in unadjusted analyses. However, adjusted results were non-significant, possibly due to limited events. Larger prospective studies are needed to confirm these findings and optimize statin therapy for vascular access preservation.