title: Soluble Fas is a marker of peripheral arterial occlusive disease in haemodialysis patients.
abstract: BACKGROUND
  Peripheral arterial occlusive disease (PAOD) including lower-extremity and cerebrovascular atherosclerosis is a leading cause of morbidity in haemodialysis patients. Recent evidence suggests that the expression of Fas, a molecule implicated in the initiation of apoptosis in various cell types, is increased at sites of atherosclerotic plaques. However, the significance of plasma levels of the soluble form of Fas (sFas) as a marker of peripheral arterial disease has yet to be defined.
  
  
  METHODS
  The present report is based on a cross-sectional analysis of baseline data from an ongoing prospective study designed to evaluate the role of sFas as marker of PAOD in end-stage renal disease (ESRD). We evaluated the association between sFas levels and evidence of PAOD in a cohort of 107 chronic haemodialysis patients.
  
  
  RESULTS
  Compared with subjects without evidence of disease (n=56), subjects with PAOD (n=51) had significantly higher plasma levels of sFas (30.0+/-8.9 vs 26.4+/-9.5 ng/ml; P=0.04). Using multiple regression, sFas was found to be associated with PAOD independently of classical risk factors for atherosclerosis (hypercholesterolaemia, diabetes, hypertension, and smoking), markers of inflammation (e.g. C-reactive protein, intercellular cell adhesion molecule type 1), and other risk factors (e.g. age, gender). An increase of one quintile in the plasma concentration of sFas was associated with an odds ratio of PAOD of 1.69 (95% CI: 1.09--2.63, P=0.01). In addition, models that incorporated sFas were significantly better at predicting PAOD than models limited to classical risk factors for atherosclerosis, alone or in combination with CRP levels (P=0.01).
  
  
  CONCLUSIONS
  Increased plasma levels of sFas are associated with established PAOD. These results suggest that sFas may represent a novel and independent marker of atherosclerosis.
authors.affiliation: Division of Nephrology, CHUS, Université de Sherbrooke, Montréal, Québec, Canada.
authors.forename: Mélanie
authors.initials: M
authors.lastname: Masse
authors.forename: Marie-Josée
authors.initials: MJ
authors.lastname: Hébert
authors.forename: Stéphan
authors.initials: S
authors.lastname: Troyanov
authors.forename: Normand
authors.initials: N
authors.lastname: Vigneault
authors.forename: Isabelle
authors.initials: I
authors.lastname: Sirois
authors.forename: François
authors.initials: F
authors.lastname: Madore
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001157:Arterial Occlusive Diseases / Q000097:blood / Q000209:etiology* / Q000276:immunology*; D001161:Arteriosclerosis / Q000097:blood / Q000209:etiology / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007376:Interleukin-2 / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications / Q000276:immunology; D008297:Male; D008875:Middle Aged; D016491:Peripheral Vascular Diseases / Q000097:blood / Q000209:etiology* / Q000276:immunology*; D006435:Renal Dialysis / Q000009:adverse effects*; D012307:Risk Factors; D012995:Solubility; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D019014:fas Receptor / Q000097:blood*
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D007376:Interleukin-2; D019010:Vascular Cell Adhesion Molecule-1; D019014:fas Receptor; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein