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Nephrol Dial Transplant (2002) 17: 958-961
© 2002 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Is FGF23 the long sought after phosphaturic factor phosphatonin?

Caroline Silve and Laurent Beck

INSERM U426 and Institut Fédératif de Recherche ‘Cellules Epithéliales’, Faculté de Médecine Xavier Bichat, Paris, France

Keywords: FGF23; phosphatonin; renal phosphate reabsorption

Genetic defects in familial hypophosphataemias associated with low renal phosphate reabsorption

The kidney is the principal organ responsible for phosphate homeostasis. It regulates serum phosphate by modulating phosphate reabsorption. This process takes place in the renal proximal tubule and is regulated by dietary phosphate and PTH. A large amount of evidence designates the sodium-phosphate cotransporter NPT2a activity as the rate limiting and regulated step in phosphate reabsorption [1,2]. Thus, NPT2a has been considered an attractive candidate gene in familial hypophosphataemia associated with low renal phosphate reabsorption. However, no familial hypophosphataemia due to a primary decrease in renal phosphate reabsorption has yet been associated with a defect in the NPT2a gene. X-linked hypophosphataemic rickets (XLH) is associated with mutations in the PHEX gene [3] (Table 1Go). Mutations in the coding region of the NPT2a gene have been excluded in hereditary hypophosphataemic rickets with hypercalciuria (HHRH) [4,5] (and the gene defect is . . . [Full Text of this Article]

Fibroblast growth factor 23 (FGF23)

FGF23 and ADHR

FGF23, TIO and XLH

FGF23, a phosphaturic hormone

Although attractive, how solid is the theory?

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