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

Hamish Dobbie1, Robert J Unwin, Nuno J R Faria

  • 1Department of Physiology and Centre for Nephrology, University College London, Hampstead Campus, Rowland Hill Street, London NW3 2PF, UK.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|November 27, 2007
PubMed
Abstract

Insights

Matrix extracellular phosphoglycoprotein (MEPE) increases phosphate excretion by reducing kidney reabsorption. This finding supports MEPE

Area of Science:

  • Biochemistry
  • Nephrology
  • Endocrinology

Background:

  • Matrix extracellular phosphoglycoprotein (MEPE) is a phosphatonin implicated in oncogenic hypophosphataemia.
  • MEPE's role in renal phosphate reabsorption is largely uncharacterized.
  • Fibroblast growth factor-23 (FGF23) is a well-known phosphatonin, but MEPE's function remains less understood.

Purpose of the Study:

  • To investigate the effect of MEPE on renal tubular phosphate reabsorption.
  • To determine if MEPE influences phosphate excretion in vivo.

Main Methods:

  • A renal clearance study was conducted in anesthetized rats.
  • Varying doses of MEPE were administered intravenously.
  • Glomerular filtration rate and phosphate excretion were measured.

Main Results:

  • MEPE did not affect glomerular filtration rate (inulin clearance).
  • MEPE administration led to rapid, dose-dependent increases in phosphate excretion.
  • Phosphate excretion increase was due to reduced tubular reabsorption.

Conclusions:

  • MEPE significantly impacts renal phosphate handling.
  • These findings support MEPE's role in the phosphaturia observed in oncogenic hypophosphataemia and rickets.

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