title: Association of serum calcitonin with coronary artery disease in individuals with and without chronic kidney disease.
abstract: BACKGROUND
  Cardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD). Recent data implicate disordered bone and mineral metabolism, including changes in serum levels of calcium, phosphate, parathyroid hormone (PTH), vitamin D, fibroblast growth factor-23 (FGF-23), and fetuin A, as novel risk factors for arterial calcification. The potential role of calcitonin, another hormonal regulator of mineral and bone metabolism, has not been studied in detail.
  
  
  METHODS
  We investigated the link between serum calcitonin and the total burden of coronary artery disease (CAD) using the validated Gensini score, in a cross-sectional study of 88 patients with estimated GFR (eGFR) between 46 and 87 ml/min/1.73 m² who underwent coronary angiography. We evaluated the associations between serum calcitonin, minerals (calcium, phosphate), calcium × phosphate product, and other factors that regulate mineral metabolism (intact PTH, 25-OH-vitamin D, FGF-23, and fetuin A) and the severity of CAD.
  
  
  RESULTS
  The mean serum calcitonin was 11.5 ± 7.8 pg/ml. In univariate analysis, the Gensini CAD severity score correlated significantly with male gender, eGFR, and serum levels of 25-OH-vitamin D, iPTH, FGF-23, fetuin A, and calcitonin (R = 0.474, P = 0.001 for the latter). In multivariate analysis adjusted for calcium, phosphate, 25-OH-vitamin D, iPTH, FGF 23, fetuin A, and calcitonin, only calcitonin (β = 0.20; P = 0.03), FGF-23, fetuin A, and 25-OH-vitamin D emerged as independent predictors of Gensini score. In the second step, we adjusted for the presence of traditional risk factors, proteinuria, and GFR. After these adjustments, the FGF-23 and fetuin A remained statistically significant predictors of the Gensini score, while calcitonin did not.
  
  
  CONCLUSIONS
  Our study suggests that, in addition to other well-known components of mineral metabolism, increased calcitonin levels are associated with greater severity of CAD. However, this relation was not independent of traditional and nontraditional cardiovascular risk factors. Longitudinal studies in larger populations including patients with more advanced CKD are needed.
authors: Department of Medicine, Division of Nephrology, Fatih University School of Medicine, Ankara, Turkey. drkanbay@yahoo.com
authors: Mehmet
authors: M
authors: Kanbay
authors: Myles
authors: M
authors: Wolf
authors: Yusuf
authors: Y
authors: Selcoki
authors: Yalcin
authors: Y
authors: Solak
authors: Mustafa
authors: M
authors: Ikizek
authors: Sema
authors: S
authors: Uysal
authors: Liviu
authors: L
authors: Segall
authors: Ferah
authors: F
authors: Armutcu
authors: Beyhan
authors: B
authors: Eryonucu
authors: Murat
authors: M
authors: Duranay
authors: David
authors: D
authors: Goldsmith
authors: Adrian
authors: A
authors: Covic
mesh_terms: D015415:Biomarkers / Q000097:blood; D002116:Calcitonin / Q000097:blood*; D003324:Coronary Artery Disease / Q000097:blood* / Q000453:epidemiology / Q000209:etiology; D003430:Cross-Sectional Studies; D005260:Female; D000089703:Fibroblast Growth Factor-23; D006801:Humans; D015994:Incidence; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012307:Risk Factors; D015996:Survival Rate / Q000639:trends
chemical_list: D015415:Biomarkers; C000717427:FGF23 protein, human; D000089703:Fibroblast Growth Factor-23; D002116:Calcitonin