title: Serum fetuin-a concentration and endothelial dysfunction in chronic kidney disease.
abstract: BACKGROUND
  Defective endothelial function, an initial step in the development of atherosclerotic plaque, is prevalent in moderate to advanced chronic kidney disease (CKD). In this study, the investigators hypothesized that fetuin-A, a calcification inhibitor, is a novel risk factor for the development of endothelial dysfunction in patients.
  
  
  METHODS
  198 nondiabetic patients with a mean age of 44.0 +/- 12.4 years and with different stages of CKD were studied. In addition to a detailed metabolic panel, flow-mediated dilatation assessed by high-resolution brachial ultrasonography was performed to determine endothelial dysfunction. Carotid intima-media thickness was also estimated by ultrasonography. Serum fetuin-A concentrations were determined by using a human ELISA method.
  
  
  RESULTS
  Endothelial dysfunction was observed in all stages (1-5) of CKD and worsened in parallel to the reduction in estimated glomerular filtration rate. Serum fetuin-A concentrations were also found to be decreased in all but stage 1 CKD. On multiple regression analysis, endothelial dysfunction was independently associated with fetuin-A (beta = 0.745, p < 0.001) and intact parathyroid hormone concentrations (beta = -0.216, p < 0.001).
  
  
  CONCLUSIONS
  These data in a selected cohort of CKD patients indicate that fetuin-A may be one of the contributing factors for the development of endothelial dysfunction in CKD patients.
authors.affiliation: Department of Nephrology, Gülhane School of Medicine, Ankara, Turkey. kaysercaglar@yahoo.co
authors.forename: Kayser
authors.initials: K
authors.lastname: Caglar
authors.forename: Mahmut Ilker
authors.initials: MI
authors.lastname: Yilmaz
authors.forename: Mutlu
authors.initials: M
authors.lastname: Saglam
authors.forename: Erdinc
authors.initials: E
authors.lastname: Cakir
authors.forename: Selim
authors.initials: S
authors.lastname: Kilic
authors.forename: Alper
authors.initials: A
authors.lastname: Sonmez
authors.forename: Tayfun
authors.initials: T
authors.lastname: Eyileten
authors.forename: Mujdat
authors.initials: M
authors.lastname: Yenicesu
authors.forename: Yusuf
authors.initials: Y
authors.lastname: Oguz
authors.forename: Mustafa
authors.initials: M
authors.lastname: Tasar
authors.forename: Abdulgaffar
authors.initials: A
authors.lastname: Vural
authors.forename: T Alp
authors.initials: TA
authors.lastname: Ikizler
authors.forename: Peter
authors.initials: P
authors.lastname: Stenvinkel
authors.forename: Bengt
authors.initials: B
authors.lastname: Lindholm
mesh_terms: D000328:Adult; D001161:Arteriosclerosis / Q000097:blood* / Q000150:complications*; D015415:Biomarkers / Q000097:blood; D001798:Blood Proteins / Q000032:analysis*; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications*; D008297:Male; D060749:alpha-2-HS-Glycoprotein
chemical_list: C556354:AHSG protein, human; D015415:Biomarkers; D001798:Blood Proteins; D060749:alpha-2-HS-Glycoprotein