title: Soluble TWEAK level: is it a marker for cardiovascular disease in long-term hemodialysis patients?
abstract: BACKGROUND
  Reduced soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) levels follow declining renal function, are strongly associated with endothelial dysfunction and predict cardiovascular events in nondialyzed chronic kidney disease patients. In contrast, elevated levels of sTWEAK predict poor survival in hemodialysis (HD) patients. Recent evidence suggests a role for sTWEAK in the pathophysiology of vascular calcification. The aim of the study was to investigate plausible links between sTWEAK, atherosclerosis, arterial stiffness and vascular calcification in HD patients.
  
  
  METHODS
  Coronary artery calcification score (CACs) determined by multislice computed tomography, arterial stiffness by pulse wave velocity (PWV) and carotid artery intima-media thickness (CA-IMT) by carotid Doppler ultrasonography were assessed in 131 long-term prevalent HD patients. sTWEAK levels were measured by ELISA (Bender MedSystems, Vienna, Austria).
  
  
  RESULTS
  Mean serum sTWEAK level was 237.0 ± 147.5 pg/mL (range 78-937). sTWEAK level was inversely correlated with CA-IMT at a borderline significance (r=-0.168, p=0.05). Neither carotid-radial PWV nor carotid-femoral PWV values correlated with sTWEAK. sTWEAK level was higher in patients with severe vascular calcification (CACs ≥400) compared to patients with CACs <400 (264.5 ± 146.8 pg/mL vs. 205.04 ± 122.4 pg/mL, p=0.02).The association between sTWEAK and vascular calcification persisted after multivariate adjustment.
  
  
  CONCLUSIONS
  There exists a weak inverse correlation between sTWEAK and carotid atherosclerosis and a positive correlation with coronary artery calcification in long-term HD patients. Our data give support for a role for sTWEAK in the pathogenesis of vascular injury in HD patients.
authors.affiliation: Division of Nephrology, Ege University School of Medicine, Izmir, Turkey. ozkangungor@yahoo.com.tr
authors.forename: Ozkan
authors.initials: O
authors.lastname: Gungor
authors.forename: Fatih
authors.initials: F
authors.lastname: Kircelli
authors.forename: Gulay
authors.initials: G
authors.lastname: Asci
authors.forename: Juan Jesus
authors.initials: JJ
authors.lastname: Carrero
authors.forename: Erhan
authors.initials: E
authors.lastname: Tatar
authors.forename: Meltem Sezis
authors.initials: MS
authors.lastname: Demirci
authors.forename: Süreyya Süha
authors.initials: SS
authors.lastname: Ozbek
authors.forename: Naim
authors.initials: N
authors.lastname: Ceylan
authors.forename: Huseyin
authors.initials: H
authors.lastname: Toz
authors.forename: Mehmet
authors.initials: M
authors.lastname: Ozkahya
authors.forename: Ercan
authors.initials: E
authors.lastname: Ok
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D050197:Atherosclerosis / Q000097:blood* / Q000150:complications; D015415:Biomarkers / Q000097:blood; D059168:Carotid Intima-Media Thickness; D003331:Coronary Vessels / Q000000981:diagnostic imaging; D000074049:Cytokine TWEAK; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D063177:Pulse Wave Analysis; D011859:Radiography; D006435:Renal Dialysis; D051436:Renal Insufficiency, Chronic / Q000097:blood* / Q000150:complications / Q000628:therapy*; D048069:Tumor Necrosis Factors / Q000097:blood*; D061205:Vascular Calcification / Q000097:blood* / Q000150:complications; D059289:Vascular Stiffness
chemical_list: D015415:Biomarkers; D000074049:Cytokine TWEAK; C109743:TNFSF12 protein, human; D048069:Tumor Necrosis Factors