肾性低磷血症:病理生理及治疗。

Clinical calcium Pub Date : 2016-02-01
Takashi Sekine
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引用次数: 0

摘要

血清磷酸盐水平受肾脏,尤其是近端肾小管的调节。近端小管中磷酸盐的跨细胞转运是通过钠依赖转运体介导的,即管腔膜上的NPT2a和NPT2b,以及基底外侧的未知通道。磷酸盐通过NPT2a和NPT2b的转运进一步受到PTH、FGF23和1,25(OH)(2)D等因子的调控。几种引起低磷血症的遗传性疾病是已知的。此外,近端小管功能障碍可发展为范可尼综合征,引起高磷尿症。在本节中,我描述了磷酸盐处理的肾脏机制和低磷血症的原因及其治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Renal hypophosphatemia:pathophysiology and treatment].

Serum level of phosphate is regulated by the kidney, especially proximal tubule. The transcellular transport of phosphate in the proximal tubule is mediated via Na dependent transporters, i.e., NPT2a and NPT2b at the luminal membrane, and unknown channel at the basolateral side. The transport of phosphate via NPT2a and NPT2b is further regulated by factors, such as PTH, FGF23, and 1,25(OH)(2)D. Several hereditary diseases that cause hypophoshatemia specically are known. In addition, dysfunction of proximal tubule may develop Fanconi syndrome, which also causes hypherphosphaturia. In this section, I describe the renal mechanisms of phosphate handling and the causes of hypophosphatemia along with its treatment.

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