酸中毒和低钾血症对肾氨代谢影响的机制。

Q3 Medicine
Electrolyte and Blood Pressure Pub Date : 2011-12-01 Epub Date: 2011-12-31 DOI:10.5049/EBP.2011.9.2.45
Ki-Hwan Han
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引用次数: 24

摘要

肾氨代谢是净酸排泄和新碳酸氢盐生成的主要组成部分。肾氨代谢受酸碱平衡调节。急性和慢性酸负荷都能促进近端小管氨的产生和尿中的分泌。相反,碱中毒减少氨生成。低钾血症是一种常见的电解质紊乱,尽管会引起代谢性碱中毒,但会显著增加肾氨的产生和排泄。尽管低钾血症的净效应与代谢性酸中毒相似,但肾氨产生和转运的分子机制尚未得到很好的理解。这篇综述总结了最近关于慢性低钾血症的肾氨代谢的研究结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Mechanisms of the effects of acidosis and hypokalemia on renal ammonia metabolism.

Mechanisms of the effects of acidosis and hypokalemia on renal ammonia metabolism.

Mechanisms of the effects of acidosis and hypokalemia on renal ammonia metabolism.

Mechanisms of the effects of acidosis and hypokalemia on renal ammonia metabolism.

Renal ammonia metabolism is the predominant component of net acid excretion and new bicarbonate generation. Renal ammonia metabolism is regulated by acid-base balance. Both acute and chronic acid loads enhance ammonia production in the proximal tubule and secretion into the urine. In contrast, alkalosis reduces ammoniagenesis. Hypokalemia is a common electrolyte disorder that significantly increases renal ammonia production and excretion, despite causing metabolic alkalosis. Although the net effects of hypokalemia are similar to metabolic acidosis, molecular mechanisms of renal ammonia production and transport have not been well understood. This mini review summarizes recent findings regarding renal ammonia metabolism in response to chronic hypokalemia.

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来源期刊
Electrolyte and Blood Pressure
Electrolyte and Blood Pressure Medicine-Internal Medicine
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