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Regulatory Mechanisms of Circulating Fibroblast Growth Factor 23 in Parathyroid Diseases
Author(s) -
Imanishi Yasuo,
Kobayashi Keisuke,
Kawata Takehisa,
Inaba Masaaki,
Nishizawa Yoshiki
Publication year - 2007
Publication title -
therapeutic apheresis and dialysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.415
H-Index - 53
eISSN - 1744-9987
pISSN - 1744-9979
DOI - 10.1111/j.1744-9987.2007.00519.x
Subject(s) - fibroblast growth factor 23 , endocrinology , medicine , hyperphosphatemia , hypophosphatemia , parathyroid hormone , vitamin d and neurology , secondary hyperparathyroidism , hyperparathyroidism , homeostasis , kidney disease , calcitriol , calcium
Abstract: Fibroblast growth factor‐23 (FGF‐23) is a circulating factor regulating phosphate and vitamin D homeostasis. Phosphate intake and an administration of 1,25‐dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ) increase circulating FGF‐23 levels, and elevated FGF‐23 prevents hyperphosphatemia and vitamin D toxicity by hyperphosphaturia and suppression of circulating 1,25(OH) 2 D level, comprising a feedback loop to maintain phosphate and vitamin D homeostasis. Excess secretion of parathyroid hormone (PTH), another phosphaturic factor, elevates the serum calcium level in primary hyperparathyroidism. PTH also elevates circulating FGF‐23 level, which cooperatively enhances the phosphaturia, resulting in hypophosphatemia. The circulating FGF‐23 level increases as renal function declines in chronic kidney disease (CKD), and it exhibits significant and positive correlations with serum phosphate, calcium, and PTH in CKD patients on maintenance hemodialysis, suggesting that these parameters regulate circulating FGF‐23 level. Tight associations between circulating FGF‐23 and calcium levels were observed both in patients with primary hyperparathyroidism and in CKD patients on maintenance hemodialysis, suggesting the role of serum calcium on FGF‐23 regulatory mechanisms. FGF‐23 may have a physiological role in preventing tissue damage such as ectopic calcifications, partly via suppressing the serum calcium × phosphate product by accelerating urinary phosphate excretion and suppressing vitamin D activation.