FIGURE 1: Rate of CRBSI. 2. Broom J, Woods M, Allworth A et al. Ethanol lock therapy to treat tunnelled central venous catheter associated blood stream infections: Results from a prospective trial. Scand J Infect Dis 2008; 40: 399–406 3. Cober MP, Kovacevich DS, Teitelbaum DH. Ethanol lock therapy for the prevention of central venous access device infections in pediatric patients with intestinal failure. J Parenter Enteral Nutr 2011; 35: 67–73 4. Broom JK, Krishnasamy R, Hawley CM et al. A randomised controlled trial of Heparin vs ETHAnol Lock THerapY for the prevention of Catheter Associated infecTion in Haemodialysis patients—the HEALTHY-CATH trial. BMC Nephrol 2012; 2: 146 5. Vercaigne LM, Allan DR, Armstrong SW et al. An ethanol/sodium citrate locking solution compared to heparin to prevent hemodialysis catheter related infections: A randomized pilot study. J Vasc Access 2016; 17: 55–62 MO789 THE EFFECT OF ORAL VITAMIN K2 VERSUS K1 ON VASCULAR CALCIFICATION IN HEMODIALYSIS PATIENTS : A RANDOMIZED CONTROLLED TRIAL Howayda El Shinnawy 1 , Tamer Elsaid 1 , Sarah Farid 2 , Ahmed Shamseldin 1 , Sherin Ibrahim 1 and Reem Elsharabasy 1 1 Faculty of Medicine, Ain Shams University, Internal medicine and Nephrology, Cairo, Egypt and 2 Faculty of Pharmacy, Ain Shams University, Clinical pharmacy, Cairo, Egypt BACKGROUND AND AIMS: Vascular calcifcation is a common complication of end-stage renal disease and an important cause of cardiovascular diseases and mortality. Vitamin K is essential for the activation of matrix Gla protein (MGP), a powerful inhibitor of tissue calcifcation. However, there are limited data on the efcacy and safety of diferent vitamin K forms on vascular calcifcation in hemodialysis patients, most of whom are essentially vitamin K defcient. METHOD: A prospective, randomized, placebo-controlled clinical trial, that included 120 eligible hemodialysis patients who were randomly assigned to one of three equal study groups: vitamin K1 (10 mg phytomenadione thrice-weekly), vitamin K2 (90 ug daily), or placebo for 3 months. Serum MGP, calcium, phosphorus, their product and intact parathyroid hormone (iPTH) levels were all assessed at baseline and at the end of the study. RESULTS: MGP levels showed a signifcant increase in the vitamin K2 group (700%) compared with (78%) and (40%) in vitamin K1 and placebo groups respectively. No change was found in bone profle at 3 months compared with baseline at both of the treatment groups. No correlations between calcium, phosphorous and PTH and MGP levels at baseline or after treatment. None of the treatment group patients experienced any adverse efects. CONCLUSION: Vitamin K supplementation was tolerable and efective in improving levels of a potent calcifcation inhibitor as MGP, with K2 form showing superiority over K1 in their impact on MGP levels among hemodialysis patients. MO790 ARTERIOVENOUS FISTULA CALCIFICATIONS—RISK FACTORS AND IMPACT ON ARTERIOVENOUS FISTULA FUNCTIONALITY Iulia Dana Grosu 1,2 , Oana Stirbu 2 , Florica Gadalean 1,2 , Flaviu Bob 1,2 , Adelina Mihaescu 1,2 , Luciana Marc 1,2 , Lazar Chisavu 12 , Oana-Marina Schiller 2 , Mircea Tandrau 2 and Adalbert Schiller 1 1 ’Victor Babes’ University of Medicine and Pharmacy Timisoara, Nephrology, Romania and 2 B. Braun Medical S.R.L., Romania BACKGROUND AND AIMS: Vascular calcifcations have been recognized as frequent fndings in patients with end-stage renal disease (ESRD) and have intricate mechanisms, including chronic kidney disease—mineral and bone disorders (CKD- MBD), infammation and advanced atherosclerosis. The pathogenesis of arteriovenous fstula (AVF) calcifcations 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 calcifcations 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 calcifcations (defned 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 calcifcations. Laboratory parameters were analysed in the same month (Hb, calcium, phosphorus, serum bicarbonate, iPTH, albumin, ferritin, CRP). Dialysis efciency (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 calcifcations was 38% (66/174). Signifcantly more radiocephalic AVFs (47%) had calcifcations than brachio-cephalic (38%) or brachio-basilic AVFs (15%), P = 0.04. The presence of calcifcations 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 calcifcations was not signifcantly associated with age, cardiac calcifcations, or the presence of diabetes mellitus. Moreover, there was no statistically signifcant diference between the eKT/v values obtained in the group with AVF calcifcations versus without AVF calcifcations. We used the Cox proportional hazards model adjusted for standardized predicted values to determine whether patients with AVF calcifcations had an increased risk of AVF failure. We found that after 1 year, 18,1% AVFs with calcifcations had failed (12/66) while only 4.6% AVFs without calcifcations had failed (5/108) [P = 0.02, hazard ratio (HR) 3.5, 95% confdence interval (95% CI) 1–11.3]. CONCLUSION: The prevalence of AVF calcifcations was 38% and afects radio- cephalic AVFs the most. AVF calcifcations detected through ultrasound represent a risk factor for AVF failure, but the mechanism might be diferent from the pathways i568 Abstract Downloaded from https://academic.oup.com/ndt/article/37/Supplement_3/gfac080.027/6577713 by guest on 17 October 2022