Fibroblast growth factor-23 (FGF-23) is independently correlated to aortic calcification in haemodialysis patients

Abstract

Background. Vascular calcification has detrimental consequences on chronic kidney disease (CKD) patients, yet its pathogenesis is not fully understood. Fibroblast growth factor-23 (FGF-23) is involved in the regulation of mineral metabolism which may in turn affect vascular calcification. Data on the relationship between FGF-23 and peripheral vascular calcification, using conventional radiographs, are conflicting, and less is known about its relation to aortic calcification. We conducted this study to investigate the relationship between FGF-23 and aortic calcification in a standard haemodialysis setting.Methods. The study included 65 haemodialysis patients (46 prevalent and 19 incident) on a three times 4-h dialysis schedule as well as 15 controls. Those with diabetes, oral anticoagulation or parathyroidectomy were excluded. Intact FGF-23, parathormone, lipids, calcium and phosphorus were measured. Aortic calcification index (ACI) was assessed by a non-contrast computerized tomography (CT) of the abdominal aorta.Results. FGF-23 levels were higher among haemodialysis patients (4681.3 ± 3906.1pg/mL) compared to controls (98.2 ± 51.9pg/mL), P = 0.005. ACI was higher in haemodialysis patients (14.1 ± 12) than controls (3.2 ± 3.6), P = 0.009. FGF-23 (P < 0.0001) and systolic blood pressure (BP) (P < 0.0001) were independently related to ACI in stepwise multiple regression analysis of pooled analysis of haemodialysis patients, R = 0.476; in subgroup analysis, the independent factors relating to ACI among prevalent dialysis patients were systolic BP (P < 0.0001), FGF-23 (P = 0.002) and age (P = 0.012), R=0.48; whereas in incident patients, only FGF-23 was associated with ACI (P = 0.007), R = 0.37.Conclusions. In haemodialysis patients, FGF-23 and ACI were significantly increased, and FGF-23 was independently associated with aortic calcification. © The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.