English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Accessible online at: www.karger.com/journals/nef Dear Sir, Patients with chronic renal failure (CRF) who require regular hemodialysis, may present vascular access thrombosis [1]. A broad spectrum of possible pathogenic mechanisms has been proposed: hemodynamic mechanisms [2], inherited thrombophilias [3] and immune etiologies. With respect to the latter, antiphospholipid antibodies (aPL) have been studied, but the role of these antibodies in the pathogenesis is controversial [4]. The aim of the present study was to analyze the prevalence of aPL antibodies and its correlation with vascular access thrombotic events. The studied population consisted of 208 consecutive CRF patients undergoing hemodialysis (112 females and 96 males; 53 B 18 years; time in hemodialysis was 35 B 29 months). In 77 patients was possible to collect a second a sample (6–18 months later). The most frequent etiologies were: diabetic nephropathy (20.2%), nephrosclerosis (15.9%) and chronic glomerulonephritis (14.4%). None of the patients had systemic lupus erythematosus (SLE) or other autoimmune disease known to be associated with aPL. All patients had arterious venous fistula (AVF) as the initial vascular access, use unfractionated heparin and cuprophane membrane filters. The thrombosis of vascular access was assessed by clinical patterns and flebography. The control group included 110 healthy blood donors and 28 CRF patients without hemodialysis. Antiphospholipid antibodies were determined by a home made solid-phase enzymelinked immunosorbent assays (anticardiolipin antibodies, aCL; antiphosphatidylserine antibodies, aPS and anti-beta-2-glycoprotein I antibodies, anti-s2GPI); a sample was considered positive when OD405 was greater than 3 SD above the average of the normal controls (cut off). The activity of the antibodies was expressed as the ratio: OD405 patient sample/ OD405 of cut off. Additionally, the aPL were determined as lupus anticoagulant activity by coagulation assays (dilute tissue thromboplastin inhibition, dTTI and kaolin clotting time, KCT). Fourteen of 208 patients (6.7%) presented aCL, 10 (4.8%) aPS and 9 (4.3%) antis2GPI. The prevalences between hemodialysis patients and normal controls were not statistically significant (table 1). In the secTable 1. Anticardiolipin, antiphosphatidylserine and anti-s2GPI antibodies in patients undergoing chronic hemodialysis and normal controls

Vascular Access Thrombosis Is Not Related to Presence of Antiphospholipid Antibodies in Patients on Chronic Hemodialysis