Kidney and Metabolic Bone Diseases Vol.15 No.4(5)

Theme Topics in calcium and phosphate transport
Title Discovery of a novel circulatory factor controlling renal phosphate transport
Publish Date 2002/10
Author Takeyoshi Yamashita Pharmaceutical Research Labs, Pharmaceutical Division, Kirin Brewery Co. Ltd.
[ Summary ] The presence of a putative circulatory hormone that regulates renal phosphate excretion has been proposed to explain disruptions of mineral metabolism in X-linked hypophosphatemic rickets and tumor-induced osteomalacia (TIO). Recently, FGF-23 was identified as a causative factor of TIO. On the other hand, genetic studies indicated that missense mutations of FGF-23 are responsible for autosomal dominant hypophosphatemic rickets/osteomalacia (ADHR). It is suggested that missense mutations of FGF-23 cause ADHR through a gain-of-function mechanism. Recent development of assay systems to measure FGF-23 concentration have contributed to our understanding of the physiological role of FGF-23. In contrast to these lines of the evidence, the assessment of the biological activity of FGF-23 in vitro is still controversial. Further studies are needed to clarify how FGF-23 regulates renal phosphate transport.
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