FP545
THE CLINICAL IMPACT OF FIBROBLAST GROWTH FACTOR 23 AND SCLEROSTIN ON VASCULAR CALCIFICATION IN PREVALENT HEMODIALYSIS PATIENTS

INTRODUCTION AND AIMS: Patients with end-stage renal disease (ESRD) experienced vascular calcification (VC), which is associated with cardiovascular disease. VC results from a phenotypic conversion of vascular smooth muscle cells into an osteoblast-like phenotype that involves osteoblast transcriptional activation proteins, such as fibroblast growth factor 23 (FGF23) and sclerostin, via a Wnt-dependent mechanism. Herein, we investigate the association between FGF23, sclerostin, and vascular calcification using a hemodialysis (HD) cohort in Taiwan.

METHODS: HD patients were enrolled from two hospital HD units. All patients received regular HD 3-4 hours using high flux dialyzers three times per week. The serum FGF23 and sclerostin concentrations were measured by luminex multiplex technology (Bone Hormone Panel, Millipore Corporation, Billerica, MA, USA). Vascular calcification was evaluated by two independent observers using chest radiographs to calculate grading aortic arch calcification (AAC) score. Two types AAC score were used, including scales divided into 4 circumferences (AAC4 score) and 16 circumferences (AAC16 score).

RESULTS: Total 341 prevalent HD patients were investigated with mean age 59.2 ± 11.5 years, 53.4% male, 41.9% diabetes mellitus, and 75.1% hypertension. Using multiple linear regression models, FGF23 concentrations were positive correlated with AAC4 score (β coefficient [β]: 0.069, 95% confidence interval [95% CI]: 0.008 − 0.130, P = 0.026) and AAC16 score (β: 0.22, 95% CI: 0.0027 − 0.44, P = 0.05) after controlling diabetes, hypertension, ischemic heart disease, hyperlipidemia, gout, and osteoporosis. In contrast, sclrostin concentrations were negative correlated with AAC4 score (β: -0.31, 95% CI: -0.52 − -0.11, P = 0.003) and AAC16 score (β: -1.02, 95% CI: -1.73 − -0.30, P = 0.005) after comorbidities adjustment.

CONCLUSIONS: In our prevalent HD cohorts, serum FGF23 levels were positive association with VC. As for the sclerostin, there was an inverse association between vascular calcification and serum sclerostin levels. Further large scale cohorts were still needed to confirm our findings.