[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.