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[肾性低磷血症:病理生理学与治疗]

[Renal hypophosphatemia:pathophysiology and treatment].

作者信息

Sekine Takashi

机构信息

Department of Pediatrics, Toho University Ohashi Hospital, Japan.

出版信息

Clin Calcium. 2016 Feb;26(2):284-94.

Abstract

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.

摘要

血清磷酸盐水平由肾脏调节,尤其是近端小管。近端小管中磷酸盐的跨细胞转运是通过钠依赖性转运体介导的,即位于管腔膜的NPT2a和NPT2b,以及位于基底外侧的未知通道。通过NPT2a和NPT2b的磷酸盐转运进一步受甲状旁腺激素、成纤维细胞生长因子23和1,25(OH)₂D等因素调节。已知有几种遗传性疾病会特异性地导致低磷血症。此外,近端小管功能障碍可能会发展为范科尼综合征,这也会导致低磷性血尿。在本节中,我将描述肾脏处理磷酸盐的机制、低磷血症的病因及其治疗方法。

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