title: Inflammation, endothelial dysfunction, and platelet activation in patients with chronic kidney disease: the chronic renal impairment in Birmingham (CRIB) study.
abstract: BACKGROUND
  Studies in the general population suggest that low-grade inflammation, endothelial dysfunction, and platelet activation are associated with an increased risk of cardiovascular events.
  
  
  METHODS
  Markers of inflammation, endothelial dysfunction, and platelet activation were measured in 334 patients with chronic kidney disease (serum creatinine >1.47 mg/dL [>130 micromol/L] at screening) and compared with 2 age- and sex-matched control groups, 1 comprising 92 patients with coronary artery disease and the other comprising 96 apparently healthy individuals with no history of cardiovascular or kidney disease.
  
  
  RESULTS
  There was evidence of low-grade inflammation in the chronic renal impairment group compared with healthy controls, with higher concentrations of C-reactive protein (3.70 versus 2.18 mg/L, P < 0.01) and fibrinogen (3.48 versus 2.67 g/L, P < 0.001) and lower serum albumin concentration (41.8 versus 44.0 g/dL [418 versus 440 g/L], P < 0.001). More severe renal impairment was associated with a trend towards higher fibrinogen and lower albumin concentrations (both P < 0.001), although there was no association with higher C-reactive protein level. As compared to healthy controls, plasma von Willebrand factor (142 versus 108 IU/dL, P < 0.001) and soluble P-selectin concentrations (57.0 versus 43.3 ng/mL, P < 0.001) were also higher in the chronic renal impairment group. More severe renal impairment was associated with a trend towards higher levels of von Willebrand factor (P < 0.001) and of soluble P selectin (P < 0.05).
  
  
  CONCLUSIONS
  This cross-sectional analysis demonstrates that chronic kidney disease is associated with low-grade inflammation, endothelial dysfunction, and platelet activation, even among patients with moderate renal impairment.
authors.affiliation: Clinical Trial Service Unit, University of Oxford, Oxford, UK. martin.landray@ctsu.ox.ac.uk
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Landray
authors.forename: David C
authors.initials: DC
authors.lastname: Wheeler
authors.forename: Gregory Y H
authors.initials: GY
authors.lastname: Lip
authors.forename: David J
authors.initials: DJ
authors.lastname: Newman
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Blann
authors.forename: Fiona J
authors.initials: FJ
authors.lastname: McGlynn
authors.forename: Simon
authors.initials: S
authors.lastname: Ball
authors.forename: John N
authors.initials: JN
authors.lastname: Townend
authors.forename: Colin
authors.initials: C
authors.lastname: Baigent
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000378:metabolism; D003324:Coronary Artery Disease / Q000503:physiopathology*; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation / Q000502:physiology*; D012709:Serum Albumin / Q000378:metabolism; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D019007:P-Selectin; D012709:Serum Albumin; D014841:von Willebrand Factor; D005340:Fibrinogen; D002097:C-Reactive Protein