Kidney and Metabolic Bone Diseases Vol.17 No.4(8)

Theme Progress in the management of phosphorus in chronic kidney disease
Title Phosphatonin and phosphate metabolism in renal failure
Publish Date 2004/10
Author Takeyoshi Yamashita Pharmacentical Research Laboratories, pharmacentical Division, KIRIN Brewery Co., Ltd.
[ Summary ] Fibroblast growth factor (FGF)-23 was cloned as a causative factor, phosphatonin, for hypophosphatemic rickets/osteomalacia. Recent studies demonstrated that FGF-23 is an important factor in the regulation of type IIa sodium-phosphate cotransporter and 25-hydroxyvitamin D-1α-hydroxylase. Serum concentrations of FGF-23 increase according to the progression of renal insufficiency in chronic kidney disease and reach extremely high levels in end-stage renal disease. FGF-23 seems to increase urinary phosphate excretion to avoid hyperphosphatemia during the early phase of renal insufficiency. Serum concentrations of FGF-23 further increase even after the severe impairment of renal function and such high serum levels of FGF-23 may contribute to the development of some complication associate with renal insufficiency.
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