Dobbie Hamish, Unwin Robert J, Faria Nuno J R, Shirley David G
Department of Physiology and Centre for Nephrology, University College London, Hampstead Campus, Rowland Hill Street, London NW3 2PF, UK.
Nephrol Dial Transplant. 2008 Feb;23(2):730-3. doi: 10.1093/ndt/gfm535. Epub 2007 Nov 23.
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.
A renal clearance study was performed in anaesthetized rats infused intravenously with a range of doses of MEPE.
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.
The results lend support to the hypothesis that MEPE contributes to the phosphaturia of oncogenic hypophosphataemia and of hypophosphataemic rickets.
基质细胞外磷酸糖蛋白（MEPE）最初是从一名致癌性低磷血症患者的肿瘤组织中分离出来的，它是一种假定的磷调节素，受到的关注远少于成纤维细胞生长因子-23。迄今为止，其对肾小管磷重吸收的影响仍不明确。
对麻醉的大鼠进行静脉输注一系列剂量MEPE的肾脏清除率研究。
MEPE对肾小球滤过率（菊粉清除率）无影响，但导致绝对磷排泄量和分数磷排泄量迅速、剂量依赖性增加，这完全归因于磷重吸收减少。在最大剂量时，MEPE使分数磷排泄量增加超过2倍，而在时间对照组中未观察到变化。
这些结果支持了MEPE导致致癌性低磷血症和低磷性佝偻病的磷尿症这一假说。
