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氨生成增加及低钾血症对肾小管的影响。

Increased ammoniagenesis and the renal tubular effects of potassium depletion.

作者信息

O'Reilly D S

出版信息

J Clin Pathol. 1984 Dec;37(12):1358-62. doi: 10.1136/jcp.37.12.1358.

Abstract

The cause of the morphological changes and functional defects in the renal tubule seen in patients with severe potassium depletion is unknown. In man and animals potassium status is a major factor regulating ammonia synthesis in the kidney and urinary ammonium excretion. A primary effect of potassium depletion is to cause an increase in ammoniagenesis by the renal tubular cells. It is proposed that the vacuolation of the renal tubular cells and the functional defects of tubular proteinuria, polyuria, resistance to arginine vasopressin, renal resistance to the action of parathyroid hormone, and increased urinary excretion of N-acetyl-beta-glucosaminidase found in potassium depletion are secondary effects caused by high concentrations of ammonia in the renal tubular cells.

摘要

严重低钾血症患者肾小管出现形态学改变和功能缺陷的原因尚不清楚。在人和动物中,钾状态是调节肾脏氨合成和尿铵排泄的主要因素。低钾血症的主要作用是导致肾小管细胞氨生成增加。有人提出,低钾血症时肾小管细胞的空泡形成以及肾小管蛋白尿、多尿、对精氨酸加压素抵抗、肾脏对甲状旁腺激素作用的抵抗,以及N-乙酰-β-氨基葡萄糖苷酶尿排泄增加等功能缺陷,是肾小管细胞内高浓度氨引起的继发效应。

相似文献

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Cellular and molecular basis of increased ammoniagenesis in potassium deprivation.钾缺乏时氨生成增加的细胞和分子基础。
Am J Physiol Renal Physiol. 2011 Nov;301(5):F969-78. doi: 10.1152/ajprenal.00010.2011. Epub 2011 Jul 27.

本文引用的文献

1
Blood ammonia.血氨
Biochem J. 1939 Apr;33(4):457-78. doi: 10.1042/bj0330457.

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