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NDT Advance Access first published online on November 23, 2007
This version published online on November 23, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm535
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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


Matrix extracellular phosphoglycoprotein causes phosphaturia in rats by inhibiting tubular phosphate reabsorption

Hamish Dobbie, Robert J. Unwin, Nuno J. R. Faria and David G. Shirley

Department of Physiology and Centre for Nephrology, University College London, Hampstead Campus, Rowland Hill Street, London NW3 2PF, UK

Correspondence and offprint requests to: Dr David G. Shirley, Department of Physiology and Centre for Nephrology, University College London, Hampstead Campus, Rowland Hill Street, London NW3 2PF, UK. Email: david.shirley{at}ucl.ac.uk



  Abstract

Background. Matrix extracellular phosphoglycoprotein (MEPE), first isolated from tumour-derived tissue from a patient with oncogenic hypophosphataemia, is a putative phosphatonin that has received much less attention than fibroblast growth factor-23. To date, its effect on renal tubular phosphate reabsorption remains undefined.

Methods. A renal clearance study was performed in anaesthetized rats infused intravenously with a range of doses of MEPE.

Results. MEPE had no effect on glomerular filtration rate (inulin clearance) but caused rapid, dose-dependent increases in absolute and fractional phosphate excretion, wholly attributable to reduced phosphate reabsorption. At a maximal dose, MEPE increased fractional phosphate excretion more than 2-fold, whereas no change was observed in time controls.

Conclusion. The results lend support to the hypothesis that MEPE contributes to the phosphaturia of oncogenic hypophosphataemia and of hypophosphataemic rickets.

Keywords: kidney; phosphatonin; phosphaturia; renal clearance

Received for publication: 28. 2.07
Accepted in revised form: 10. 7.07


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