title: FGF-23 associated with the progression of coronary artery calcification in hemodialysis patients.
abstract: BACKGROUND
  Disordered mineral metabolism is implicated in the pathogenesis of vascular calcification in hemodialysis (HD) patients. Fibroblast growth factor 23 (FGF-23) is the main regulator of phosphate metabolism. In this prospective study, we aimed to investigate the association of serum FGF-23 with progression of coronary artery calcification in HD patients.
  
  
  METHODS
  Seventy-four HD patients (36 male/38 female, mean age: 52 ± 14 years) were included. Serum FGF-23 levels were measured by ELISA. Coronary artery calcification score (CACS) was measured twice with one year interval. Patients were grouped as progressive (PG) (36 patients-48%) and non-progressive (NPG).
  
  
  RESULTS
  Age, serum phosphorus, baseline and first year CACS were found to be significantly higher in the PG compared to NPG group. Serum FGF-23 levels were significantly higher in PG [155 (80-468) vs 147 (82-234), p = 0.04]. Patients were divided into two groups according to baseline CACS (low group, CACS ≤ 30; high group, CACS > 30). Serum FGF-23 levels were significantly correlated with the progression of CACS (ΔCACS) in the low baseline CACS group (r = 0.51, p = 0.006), but this association was not found in high baseline CACS group (r = 0.11, p = 0.44). In logistic regression analysis for predicting the PG patients; serum FGF-23, phosphorus levels and baseline CACS were retained as significant factors in the model.
  
  
  CONCLUSIONS
  Serum FGF-23 was found to be related to progression of CACS independent of serum phosphorus levels. FGF-23 may play a major role in the progression of vascular calcification especially at the early stages of calcification process in HD patients.
authors.forename: Abdullah
authors.initials: A
authors.lastname: Ozkok
authors.forename: Cigdem
authors.initials: C
authors.lastname: Kekik
authors.forename: Gonca Emel
authors.initials: GE
authors.lastname: Karahan
authors.forename: Tamer
authors.initials: T
authors.lastname: Sakaci
authors.forename: Alper
authors.initials: A
authors.lastname: Ozel
authors.forename: Abdulkadir
authors.initials: A
authors.lastname: Unsal
authors.affiliation: Department of Internal Medicine and Nephrology, Istanbul University, Istanbul Faculty of Medicine, Istanbul, Turkey. alayildiz@yahoo.com.
authors.forename: Alaattin
authors.initials: A
authors.lastname: Yildiz
mesh_terms: D015415:Biomarkers / Q000097:blood; D002114:Calcinosis / Q000097:blood* / Q000453:epidemiology*; D015984:Causality; D015897:Comorbidity; D003324:Coronary Artery Disease / Q000097:blood* / Q000453:epidemiology*; D018450:Disease Progression; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors; D006801:Humans; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D006435:Renal Dialysis / Q000706:statistics & numerical data*; D051436:Renal Insufficiency, Chronic / Q000097:blood* / Q000453:epidemiology / Q000534:rehabilitation*; D015203:Reproducibility of Results; D012307:Risk Factors; D012680:Sensitivity and Specificity; D014421:Turkey / Q000453:epidemiology
chemical_list: D015415:Biomarkers; C000717427:FGF23 protein, human; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23