Phosphatonins are regulatory factors of
phosphate metabolism and the FGF23 is the best studied of them. This has produced a change in our understanding in
mineral metabolism and specifically of
phosphate regulation. FGF23 is a 251-amino
acid factor that differs from other FGF family members by having a 71-amino
acid extension on the carboxyl-terminal end of the molecule that is specific for this factor. It is primarily produced by osteocytes in bone. It has a central role in
phosphate homeostasis regulation, producing
phosphaturia, and in
vitamin D metabolism, inhibiting its production by suppression of renal 1 Alfa
hydroxylase. It is believed to have an important place in the pathogenesis of early secondary hyperparathiroidism related to
chronic renal insufficiency by inhibiting renal synthesis of 1,25(
OH)2D in response to its increment in blood produced to increase renal
phosphate excretion and maintain
phosphate balance. In CRF its serum levels seem to be independent predictors of progression to terminal
renal failure. In dialysis patients the determination of its serum levels would allow to predict the results of
therapy with
calcitriol in the treatment of
secondary hyperparathyroidism; they also seem to be independent predictors of the risk of mortality during the first year of
hemodialysis. Its serum levels have also been related to the development of
vascular calcifications of hand arteries but not with aortic calcifications. The exposure to excessive levels of FGF23 in the early postransplant period seems to be strongly associated with postransplant hypophophatemia more than to PTH or other phosphatonins.