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High-Flux Hemodialysis Benefits Hemodialysis Patients by Reducing Serum FGF-23 Levels and Reducing Vascular Calcification

Xiao Fu, Qin-Qin Cui, Jian-Ping Ning, Shuang-Shuang Fu, Xiao-Hua Liao

Department of Nephrology, Xiangya Hospital, Central South University, Changsha, Hunan, China (mainland)

Med Sci Monit 2015; 21:3467-3473

DOI: 10.12659/MSM.894894

Available online:

Published: 2015-11-11

BACKGROUND: High- and low-flux hemodialysis (HFHD and LFHD, respectively) are dialysis procedures designed to eliminate blood toxins that accumulate in end-stage renal disease. HFHD may reduce vascular calcification by removing serum fibroblast growth factor 23 (FGF-23). However, whether HFHD is better than LFHD is still under debate. We therefore compared the efficacy of HFHD and LFHD in controlling FGF-23 and vascular calcification.
MATERIAL AND METHODS: Fifty hemodialysis patients were recruited and randomly treated with either HFHD or LFHD. Fasting venous blood was collected at baseline, six months, and twelve months after the treatment. We then measured levels of FGF-23, calcium, phosphorus, parathyroid hormone, and alkaline phosphatase. Further, abdominal lateral radiographs were taken to calculate aorta abdominalis calcification scores (AACs).
RESULTS: Compared to the LFHD group, FGF-23 and AACs in the HFHD group significantly decreased after 12 months treatment (p=0.049 and p=0.002, respectively). AACs were positively correlated with FGF-23 in all patients (p=0.004), the HFHD group alone (p=0.040), and the LFHD group alone (p=0.037). We also found that older patients, patients with higher blood phosphorus levels, and higher FGF-23 levels had an increased risk of aorta abdominalis calcification (p=0.048, p=0.003, p=0.001, respectively). HFHD was more able to reduce the risk of aorta abdominalis calcification than LFHD (p=0.003).
CONCLUSIONS: FGF-23 is an independent risk factor for the development of vascular calcification. HFHD may benefit hemodialysis patients by reducing serum FGF-23 levels and controlling vascular calcification.

Keywords: Alkaline Phosphatase - metabolism, Adult, Aorta, Abdominal - pathology, Calcium - blood, Fibroblast Growth Factors - blood, Gene Expression Regulation, Kidney Failure, Chronic - therapy, Parathyroid Hormone - blood, Phosphorus - blood, Radiography, Abdominal, Regression Analysis, Renal Dialysis, Renal Insufficiency, Chronic - therapy, Risk Factors, Vascular Calcification - blood