title: Increased plasma S-nitrosothiol levels in chronic haemodialysis patients.
abstract: BACKGROUND
  An impairment of nitric oxide (NO) bioavailability and/or metabolism may contribute to the excessive incidence of atherosclerotic complications observed in haemodialysis (HD) patients. Recent evidence indicates that NO metabolism involves a family of NO-related molecules that have not yet been explored in such patients. The aim of our study was to determine the plasma levels of S-nitrosothiol and nitrotyrosine in chronic HD patients, and to evaluate potential factors influencing their levels.
  
  
  METHODS
  Plasma levels of S-nitrosothiols and nitrotyrosine were determined in 22 non-smoking HD patients and 12 healthy control subjects, together with albumin, homocysteine, haemoglobin, highly sensitive C-reactive protein (hsCRP) and various components of the oxidant-antioxidant system at the plasma and erythrocyte levels.
  
  
  RESULTS
  While plasma nitrosothiol levels were significantly higher in HD patients than in controls (2.25 +/- 1.17 vs 0.45 +/- 0.45 micromol/l, respectively, P < 0.0001), nitrotyrosine levels were not different. HD patients also exhibited a marked deficit of ascorbate and low plasma glutathione peroxidase activity. An inverse relationship was found between plasma S-nitrosothiol and blood haemoglobin in HD patients (P < 0.005). No direct relationship was observed between plasma S-nitrosothiol levels and any of the oxidative stress markers, or hsCRP levels.
  
  
  CONCLUSIONS
  This study demonstrates high plasma S-nitrosothiol levels in HD patients, which are partially related to low blood haemoglobin concentrations. The pathophysiological significance of this elevation remains to be elucidated. A possible protective role against nitrosative stress is suggested in presence of normal plasma nitrotyrosine levels in such patients.
authors.affiliation: INSERM U507, Necker Hospital, Paris, France. massy@necker.fr
authors.forename: Ziad A
authors.initials: ZA
authors.lastname: Massy
authors.forename: Didier
authors.initials: D
authors.lastname: Borderie
authors.forename: Thao
authors.initials: T
authors.lastname: Nguyen-Khoa
authors.forename: Tilman B
authors.initials: TB
authors.lastname: Drüeke
authors.forename: Ohvanesse G
authors.initials: OG
authors.lastname: Ekindjian
authors.forename: Bernard
authors.initials: B
authors.lastname: Lacour
mesh_terms: D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism; D005260:Female; D005978:Glutathione / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood; D006801:Humans; D007501:Iron / Q000097:blood; D007674:Kidney Diseases / Q000150:complications; D007676:Kidney Failure, Chronic / Q000097:blood / Q000628:therapy; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D012016:Reference Values; D006435:Renal Dialysis; D026403:S-Nitrosothiols / Q000097:blood*; D014168:Transferrin / Q000378:metabolism; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000097:blood
chemical_list: D015415:Biomarkers; D026403:S-Nitrosothiols; D014168:Transferrin; D009569:Nitric Oxide; C002744:3-nitrotyrosine; D014443:Tyrosine; D002097:C-Reactive Protein; D007501:Iron; D005979:Glutathione Peroxidase; D005978:Glutathione