Renal phosphate handling in human – what can we learn from hereditary hypophosphataemias?
Article first published online: 14 APR 2010
© 2010 The Authors. Journal Compilation © 2010 Stichting European Society for Clinical Investigation Journal Foundation
European Journal of Clinical Investigation
Volume 40, Issue 6, pages 552–560, June 2010
How to Cite
Amatschek, S., Haller, M. and Oberbauer, R. (2010), Renal phosphate handling in human – what can we learn from hereditary hypophosphataemias?. European Journal of Clinical Investigation, 40: 552–560. doi: 10.1111/j.1365-2362.2010.02286.x
- Issue published online: 18 MAY 2010
- Article first published online: 14 APR 2010
- Received 11 January 2010; accepted 3 March 2010
- renal phosphate reabsorption
Eur J Clin Invest 2010; 40 (6): 552–560
Background Renal reabsorption of inorganic phosphate is critical for the maintenance of phosphate homeostasis. The sodium dependent phosphate cotransporters NaPi-IIa and NaPi-IIc have been identified to fulfill this task at the brush border membrane of proximal tubule cells. Various factors including dietary phosphate intake, parathyroid hormone, or the so called phosphatonins such as FGF23 have been shown to regulate activity of these transporters.
Design This review seeks to give an update on our current knowledge about regulatory mechanisms involved in human renal phosphate reabsorption.
Results Recently, an increasing number of genes have been identified that are directly associated with inherited phosphate wasting disorders (Klotho, PHEX, DMP1 and NHERF1). Several of these genes are predominantly expressed by osteocytes and osteoclasts in the bone suggesting indispensable signalling pathways between kidneys and the skeleton.
Conclusion In this review, the affected gene products in these inherited hypophosphataemias and their contribution to phosphate homeostasis are discussed.