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NDT Advance Access originally published online on March 29, 2007
Nephrology Dialysis Transplantation 2007 22(6):1521-1523; doi:10.1093/ndt/gfm116
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

More on the bone-kidney axis—lessons from hypophosphataemia*

Sagrario Cañadillas1, Alberto Rodríguez-Benot1 and Mariano Rodríguez1

1Research Unit and Nephrology Service, Hospital Universitario Reina Sofía, Cordoba, Spain

Correspondence and offprint requests to: Mariano Rodriguez, Unidad de Investigación, Hospital Universitario Reina Sofía, Avenida Menendez Pidal s/n. 14004 Córdoba. Spain. Email: juanm.rodriguez.sspa@juntadeandalucia.es

Keywords: high fibroblast growth factor (FGF23); hypophosphataemia; phosphaturia; dentin matrix protein 1 (DMP1)

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There are several hypophosphataemic disorders attributed to the phosphaturic effect of high fibroblast growth factor (FGF23) levels (Table 1). X-linked hypophosphatemia (XLH) is caused by inactivating mutations in a gene encoding a putative endopeptidase (PHEX) which normally cleaves the phosphaturic hormone FGF23 [1]. Both PHEX and FGF23 are abundantly expressed in bone. Inactivation of PHEX leads to excess of FGF23 which in turn causes phosphaturia, hypophosphataemia and inappropriately normal levels of 1,25(OH)2 D3 that should be high due to the hypophosphataemic stimulus of renal 1{alpha} hydroxylase activity. Autosomal dominant hypophosphataemic rickets (ADHR) are caused by mutations in the FGF23 gene that makes this phosphaturic factor resistant to proteolytic cleavage by a proprotein convertase [2]. High FGF23 is also observed in patients with certain mesenchymal tumours in which FGF23 is . . . [Full Text of this Article]



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