Choi Nak-Won
Depatment of internal Medicine, Konyang University College of Medicine, Daejeon, Korea.
Electrolyte Blood Press. 2008 Dec;6(2):77-85. doi: 10.5049/EBP.2008.6.2.77. Epub 2008 Dec 31.
The serum phosphorus level is maintained through a complex interplay between intestinal absorption, exchange intracellular and bone storage pools, and renal tubular reabsorption. The kidney plays a major role in regulation of phosphorus homeostasis by renal tubular reabsorption. Type IIa and type IIc Na(+)/Pi transporters are important renal Na(+)-dependent inorganic phosphate (Pi) transporters, which are expressed in the brush border membrane of proximal tubular cells. Both are regulated by dietary Pi intake, vitamin D, fibroblast growth factor 23 (FGF23) and parathyroid hormone. The expression of type IIa Na(+)/Pi transporter result from hypophosphatemia quickly. However, type IIc appears to act more slowly. Physiological and pathophysiological alteration in renal Pi reabsorption are related to altered brush border membrane expression/content of the type II Na(+)/Pi cotransporter. Many studies of genetic and acquired renal phosphate wasting disorders have led to the identification of novel genes. Two novel Pi regulating genes, PHEX and FGF23, play a role in the pathophysiology of genetic and acquired renal phosphate wasting disorders and studies are underway to define their mechanism on renal Pi regulation. In recent studies, sodium-hydrogen exchanger regulatory factor 1 (NHERF1) is reported as another new regulator for Pi reabsorption mechanism.
血清磷水平通过肠道吸收、细胞内交换和骨储存池以及肾小管重吸收之间的复杂相互作用来维持。肾脏通过肾小管重吸收在磷稳态调节中起主要作用。IIa型和IIc型Na(+)/Pi转运体是重要的肾脏Na(+)依赖性无机磷酸盐（Pi）转运体，它们表达于近端肾小管细胞的刷状缘膜。二者均受饮食中Pi摄入量、维生素D、成纤维细胞生长因子23（FGF23）和甲状旁腺激素的调节。低磷血症可迅速导致IIa型Na(+)/Pi转运体的表达。然而，IIc型的作用似乎较为缓慢。肾脏Pi重吸收的生理和病理生理改变与II型Na(+)/Pi共转运体刷状缘膜表达/含量的改变有关。许多关于遗传性和获得性肾性磷酸盐消耗性疾病的研究已导致发现新的基因。两个新的Pi调节基因，PHEX和FGF23，在遗传性和获得性肾性磷酸盐消耗性疾病的病理生理学中起作用，目前正在进行研究以确定它们对肾脏Pi调节的机制。在最近的研究中，钠氢交换调节因子1（NHERF1）被报道为Pi重吸收机制的另一个新调节因子。
