Latest findings in phosphate homeostasis

• Published in: Kidney international Vol. 75; no. 9; pp. 882 - 889
• Main Authors: Prié, Dominique, Torres, Pablo Ureña, Friedlander, Gérard
• Format: Journal Article
• Language: English
• Published: Basingstoke Elsevier Inc 01.05.2009; Nature Publishing Group; Elsevier Limited
• Subjects: Biological and medical sciences; FGF23; Fibroblast Growth Factors - physiology; Glucuronidase - physiology; Homeostasis - physiology; Humans; Kidney - metabolism; klotho; Medical sciences; Mutation; Nephrology. Urinary tract diseases; NHERF1; NPT2a; NPT2c; phosphate transport; Phosphate Transport Proteins - genetics; Phosphate Transport Proteins - metabolism; Phosphates - metabolism; klotho; NPT2a; NHERF1; NPT2c; phosphate transport; FGF23; Phosphates; Nephrology; Peptide hormone; Homeostasis; Kidney; Urology; Urinary system; Parathyroid hormone; Transport
• ISSN: 0085-2538; 1523-1755
• DOI: 10.1038/ki.2008.643

The kidney is a key player in phosphate balance. Inappropriate renal phosphate transport may alter serum phosphate concentration and bone mineralization, and increase the risk of renal lithiasis or soft tissue calcifications. The recent identification of fibroblast growth factor 23 (FGF23) as a hormone regulating phosphate and calcitriol metabolism and of klotho has changed the understanding of phosphate homeostasis; and a bone–kidney axis has emerged. In this review, we present recent findings regarding the consequences of mutations affecting several human genes encoding renal phosphate transporters or proteins regulating phosphate transport activity. We also describe the role played by the FGF23–klotho axis in phosphate homeostasis and its involvement in the pathophysiology of phosphate disturbances in chronic kidney disease.