title: FGF23 is independently associated with vascular calcification but not bone mineral density in patients at various CKD stages.
abstract: CONCLUSIONS
  The hormone fibroblast growth factor 23 (FGF23) is involved in mineral homeostasis but may also have a role in vascular calcification and bone mineralization. In a cohort of 142 patients with CKD stages 2-5D, plasma FGF23 was independently associated with aortic calcification but not with pulse wave velocity or bone mineral density.
  
  
  BACKGROUND
  FGF23 is involved in mineral homeostasis but may also have a role in vascular calcification and bone mineralization. Previous studies related to FGF23 and vascular and bone outcomes have been restricted to dialysis patients. The aim of the present study was to establish whether or not plasma FGF23 is associated with aortic and coronary calcification, arterial stiffness, and bone mineral density in patients with early as well as late stages of CKD.
  
  
  METHODS
  In a cohort of 142 patients with CKD stages 2-5D, we made routine biochemistry and intact FGF23 determinations, and assessed aortic and coronary calcification, bone mineral density (BMD), and arterial stiffness by multislice spiral computed tomography and automated pulse wave velocity (PWV).
  
  
  RESULTS
  Plasma intact FGF23 levels were elevated in CKD patients; the elevation preceded that of serum phosphate in early-stage CKD. Patients with elevated FGF23 levels had higher aortic and coronary calcification scores than patients with lower FGF23 levels. Multivariate linear regression analysis indicated that only age (p < 0.001) and FGF23 (p = 0.008) were independently associated with aortic calcification score. Plasma FGF23 was neither associated with PWV nor with BMD.
  
  
  CONCLUSIONS
  Our data suggest that plasma FGF23 is an independent biomarker of vascular calcification in patients with various CKD stages including early stages. The association between vascular calcification and FGF23 levels appears to be independent of BMD. It remains to be seen whether this association is independent of bone turnover and bone mass.
authors: INSERM ERI-12 (EA 4292), UFR de Médecine et Pharmacie, Jules Verne University of Picardy, Amiens, France.
authors: L
authors: L
authors: Desjardins
authors: S
authors: S
authors: Liabeuf
authors: C
authors: C
authors: Renard
authors: A
authors: A
authors: Lenglet
authors: H-D
authors: HD
authors: Lemke
authors: G
authors: G
authors: Choukroun
authors: T B
authors: TB
authors: Drueke
authors: Z A
authors: ZA
authors: Massy
mesh_terms: D000368:Aged; D001018:Aortic Diseases / Q000097:blood / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D001783:Blood Flow Velocity / Q000502:physiology; D015519:Bone Density / Q000502:physiology*; D015331:Cohort Studies; D003327:Coronary Disease / Q000097:blood / Q000209:etiology; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000097:blood / Q000502:physiology*; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D061330:Multidetector Computed Tomography / Q000379:methods; D011673:Pulsatile Flow / Q000502:physiology; D012720:Severity of Illness Index; D061205:Vascular Calcification / Q000097:blood* / Q000209:etiology; D059289:Vascular Stiffness / Q000502:physiology
chemical_list: D015415:Biomarkers; C000717427:FGF23 protein, human; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23