Fibroblast growth factor-23 and vascular calcification in chronic kidney disease and hemodialysis patients

Abstract

Context Fibroblast growth factor-23 (FGF-23) is secreted by osteoblasts and regulates phosphate and vitamin D homeostasis. As a potential explanatory mechanism of FGF-23-associated mortality, multiple studies have consistently demonstrated that higher FGF-23 levels are independently associated with greater risk of prevalent and incident left ventricular hypertrophy (LVH). In contrast, observational studies reported conflicting results on the association of FGF-23 with arterial calcification, which is another prominent pattern of cardiovascular injury in chronic kidney disease (CKD). Aims The aim was to correlate between serum FGF-23 and vascular calcification (VC) in CKD and hemodialysis (HD) patients. Settings and design A single-center cross-sectional study was conducted on 60 patients who were divided into two groups. Group I included thirty patients with CKD stages 4 and 5, and group II included thirty patients on maintenance HD. Group III included 30 age-matched and sex-matched healthy volunteers. Materials and methods Estimation of serum calcium, phosphorus, bone-specific alkaline phosphatase, intact parathyroid hormone, and serum FGF-23 level was carried out. Assessment of LVH by echocardiography and VC by multidetector computed tomography was done. Results There was a statistically significant negative correlation between FGF-23 and serum calcium level in group I and of no statistical significant correlation in group II and III, whereas there were a statistically significant positive correlations between FGF-23 with serum phosphorus, bone-specific alkaline phosphatase and intact parathyroid hormone in groups I and II and of no statistical significant correlations in group III. There were statistically significant positive correlations between FGF-23 and both left ventricular mass index and VC in groups I and II (P Conclusion FGF-23 correlates with LVH and VC in CKD and HD patients.