MO790: Arteriovenous Fistula Calcifications—Risk Factors and Impact on Arteriovenous Fistula Functionality

Abstract BACKGROUND AND AIMS Vascular calcifications have been recognized as frequent findings in patients with end-stage renal disease (ESRD) and have intricate mechanisms, including chronic kidney disease—mineral and bone disorders (CKD-MBD), inflammation and advanced atherosclerosis. The pathogenesis of arteriovenous fistula (AVF) calcifications is not fully understood, since it involves many other factors related to haemodialysis (HD) such as haemodynamic variables or vessel wall shear stress. The current study aims to assess the risk factors related to AVF calcifications and the impact on AVF functionality. METHOD The study included 174 chronic HD patients, mean age 58 ± 12 years, 35% female, median AVF duration 44 ± 52 months, with 35.9% radio-cephalic AVF, 12.1% brachio-basilic AVF, 52% brachio-cephalic AVF. The same nephrologist performed Doppler and B-mode AVF US scans in order to record AVF calcifications (defined as areas of hyperechogenicity with or without posterior shadowing within the arterial wall), as well as other complications (stenosis, partial thrombosis, aneurysms). In the same month of the AVF ultrasound assessment, cardiac echocardiography was performed in order to assess valvular calcifications. Laboratory parameters were analysed in the same month (Hb, calcium, phosphorus, serum bicarbonate, iPTH, albumin, ferritin, CRP). Dialysis efficiency (mean eKt/V in the month of ultrasound assessment) was recorded. The AVF survival was followed for 1 year after the initial evaluation, or up to the patient's death/transplantation. Statistical analysis was performed using MedCalc 14.8.1.0. RESULTS In our group, we found that the prevalence of AVF calcifications was 38% (66/174). Significantly more radiocephalic AVFs (47%) had calcifications than brachio-cephalic (38%) or brachio-basilic AVFs (15%), P = 0.04. The presence of calcifications was associated with longer AVF duration (P < .001), the presence of concomitant AVF stenosis (P = .04) and lower Hb levels (P = .02). The presence of AVF calcifications was not significantly associated with age, cardiac calcifications, or the presence of diabetes mellitus. Moreover, there was no statistically significant difference between the eKT/v values obtained in the group with AVF calcifications versus without AVF calcifications. We used the Cox proportional hazards model adjusted for standardized predicted values to determine whether patients with AVF calcifications had an increased risk of AVF failure. We found that after 1 year, 18,1% AVFs with calcifications had failed (12/66) while only 4.6% AVFs without calcifications had failed (5/108) [P = 0.02, hazard ratio (HR) 3.5, 95% confidence interval (95% CI) 1–11.3]. CONCLUSION The prevalence of AVF calcifications was 38% and affects radio-cephalic AVFs the most. AVF calcifications detected through ultrasound represent a risk factor for AVF failure, but the mechanism might be different from the pathways engaged in other vascular calcifications associated with CKD. We found no correlation with concomitant cardiac calcifications or CKD-MBD related biochemical changes. We found that AVF calcifications rather associate with HD-related factors (longer AVF duration and the presence of AVF stenosis). We suggest that periodic screening via ultrasound may be an easy method to diagnose AVF calcifications.