Role of fibroblast growth factor-23 in the pathogenesis of atherosclerosis in peritoneal dialysis patients.

Abstract

Several previous studies have demonstrated that elevated levels of fibroblast growth factor-23 (FGF-23) may be involved in atherosclerosis and contribute to the high mortality rate of peritoneal dialysis (PD) patients. The aim of this study was to determine the precise role of FGF-23 in the pathogenesis of atherosclerosis in PD patients. Between April 2009 and January 2012, 62 PD patients and 25 control subjects were included in the study. An enzyme-linked immunosorbent assay was conducted to test for plasma FGF-23 levels. Carotid artery intima-media thickness (CIMT), left ventricular mass index (LVMI), and myocardial performance index (MPI) were determined by ultrasonography. Plasma Ca(2+), P(3+), calcium-phosphorus product, parathyroid hormone, N-terminal pro-brain natriuretic peptide, and cardiac troponin I were also detected. Plasma FGF-23 levels in PD patients were significantly higher than those in control subjects. PD patients with CIMT > 1.0 mm showed the highest levels of FGF-23. Plasma P(3+), calcium-phosphorous product, plasma parathyroid hormone, CIMT, LVMI, and MPI levels were positively associated with plasma FGF-23 levels. Multiple-stepwise regression analyses revealed that plasma P(3+), plasma parathyroid hormone, CIMT, LVMI, and MPI levels were strongly associated with plasma FGF-23 levels. However, no correlations were observed in plasma N-terminal pro-brain natriuretic hormone and cardiac troponin I levels. Plasma FGF- 23 levels may play an important role in the initiation and progression of atherosclerosis. Thus, detecting and defining plasma FGF-23 levels may be a promising biomarker for the early detection of atherosclerosis in PD patients.