Dialysis – Transplantation

Kidney International (2004) 65, 1943–1946; doi:10.1111/j.1523-1755.2004.00604.x

FGF-23 in patients with end-stage renal disease on hemodialysis

Yasuo Imanishi, Masaaki Inaba, Kiyoshi Nakatsuka, Kyoko Nagasue, Senji Okuno, Asami Yoshihara, Masakazu Miura, Akimitsu Miyauchi, Keisuke Kobayashi, Takami Miki, Tetsuo Shoji, Eiji Ishimura and Yoshiki Nishizawa

Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan; Department of Nephrology, Osaka City University Graduate School of Medicine, Osaka, Japan; Shirasagi Hospital, Osaka, Japan; Mitsubishi Kagaku BCL, Osaka, Japan; National Hyogo Chuo Hospital, Hyogo, Japan; and Department of Geriatrics and Neurology, Osaka City University Graduate School of Medicine, Osaka, Japan

Correspondence: Yasuo Imanishi, M.D., Ph.D., Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. E-mail: imanishi@med.osaka-cu.ac.jp

Received 18 January 2003; Revised 3 September 2003; Re-revised 27 November 2003; Accepted 22 December 2003.

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Abstract

FGF-23 in patients with end-stage renal disease on hemodialysis.

Background

 

Fibroblast growth factor (FGF)-23 is a recently identified circulating factor which causes renal phosphate wasting disorders. Although the mechanism of regulation of FGF-23 secretion is unknown, plasma FGF-23 level may be regulated or affected by serum phosphate levels because of its hypophosphatemic effect.

Methods

 

We tested the hypothesis that plasma FGF-23 levels may be increased in hyperphosphatemia in patients with end-stage renal disease (ESRD) on maintenance hemodialysis. We measured plasma FGF-23 levels in 158 male uremic patients on maintenance hemodialysis. Plasma samples were obtained before starting dialysis sessions to determine FGF-23 levels by enzyme-linked immunosorbent assay (ELISA).

Results

 

Plasma FGF-23 level exhibited significant and positive correlations with inorganic phosphate, intact parathyroid hormone (PTH), corrected calcium, and duration of hemodialysis on simple regression analyses. All these associations remained significant in multiple regression analyses.

Conclusion

 

Serum phosphate, calcium, and intact PTH could be regulators of FGF-23 levels in uremic patients on maintenance hemodialysis. Our results may provide new insights into the pathophysiologic effects of FGF-23 on calcium-phosphate homeostasis.

Keywords:

FGF-23, phosphate, PTH, calcium, renal failure, hemodialysis

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