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高钾血症在孤立性醛固酮缺乏症代谢性酸中毒中的作用。

Role of hyperkalemia in the metabolic acidosis of isolated hypoaldosteronism.

作者信息

Szylman P, Better O S, Chaimowitz C, Rosler A

出版信息

N Engl J Med. 1976 Feb 12;294(7):361-5. doi: 10.1056/NEJM197602122940703.

Abstract

We studied the relative importance of hyperkalemia and mineralocorticoid deficiency in the metabolic acidosis of a patient with proved isolated hyporeninemic hypoaldosteronism and moderate kidney failure. The hyperkalemia and acidosis were severe in relation to the slight azotemia. Despite the systemic acidosis and urinary pH of 4.9, urinary ammonium excretion was distinctly blunted. Correction of the hyperkalemia by potassium-sodium exchange resin alone resolved the acidosis and restored the previously diminished urinary ammonium excretion to normal. Administration of mineralocorticoids only partially corrected the hyperkalemia and the acidosis. Hyperkalemia by itself, rather than hypoaldosteronism per se, caused the acidosis in this patient. Hyperkalemia apparently suppresses urinary ammonium excretion and thus interferes with urinary acidification.

摘要

我们研究了高钾血症和盐皮质激素缺乏在一名已证实患有孤立性低肾素性低醛固酮血症和中度肾衰竭患者代谢性酸中毒中的相对重要性。相对于轻微的氮质血症,高钾血症和酸中毒较为严重。尽管存在全身性酸中毒且尿pH值为4.9,但尿铵排泄明显减少。仅用钾-钠交换树脂纠正高钾血症即可缓解酸中毒,并使先前减少的尿铵排泄恢复正常。给予盐皮质激素仅部分纠正了高钾血症和酸中毒。在该患者中,高钾血症本身而非醛固酮缺乏导致了酸中毒。高钾血症显然抑制了尿铵排泄,从而干扰了尿液酸化。

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