[Biological activity of FGF-23 and pathophysiologic role in chronic kidney disease].
Recent studies indicate that FGF-23, which was originally identified as an endogenous causative factor for hypophosphatemic diseases, is a physiologic factor for the regulation of phosphate homeostasis and vitamin D metabolism. In patients with renal failure, serum concentrations of FGF-23 positively correlate with serum levels of phosphate, Ca-P product, and prathyroid hormone. It is plausible that increased FGF-23 levels are responsible for the reduction of 1,25(OH)2D levels in the early stage of renal insufficiency and also involved in the development of secondary hyperparathyroidism in chronic and end-stage kidney disease.
Yamashita
Takeyoshi
T
Pharmaceutical Research Laboratories, Pharmaceutical Division, KIRIN Brewery Co., Ltd.
D000818:Animals; D002118:Calcium / Q000097:blood; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000097:blood / Q000502:physiology*; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000209:etiology; D007014:Hypophosphatasia / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000097:blood / Q000209:etiology*; D010281:Parathyroid Hormone / Q000097:blood; D010710:Phosphates / Q000378:metabolism; D010758:Phosphorus / Q000097:blood; D014807:Vitamin D / Q000031:analogs & derivatives* / Q000097:blood / Q000378:metabolism
C000717427:FGF23 protein, human; D010281:Parathyroid Hormone; D010710:Phosphates; D014807:Vitamin D; D010758:Phosphorus; D005346:Fibroblast Growth Factors; C097949:1,25-dihydroxyvitamin D; D000089703:Fibroblast Growth Factor-23; D002118:Calcium