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实验性代谢性酸中毒中高钙尿症的机制。

Mechanism of hypercalciuria in experimental metabolic acidosis.

作者信息

Marya R K, Dadoo R C, Khurana S, Keshwani R K, Chhabra H L

出版信息

Indian J Physiol Pharmacol. 1980 Oct-Dec;24(4):341-5.

PMID:7216389
Abstract

To study the mechanism of hypercalciuria in metabolic acidosis, ammonium chloride loading (long) test was performed in 68 stone formers and 50 controls. Administration of ammonium chloride in both stone formers and controls produced a significant increase in urinary volume, ammonium and calcium excretions, no change in plasma calcium and creatinine clearance and significant decrease in plasma bicarbonate. However, on the third day of ammonium chloride loading test, urinary ammonium excretion and plasma bicarbonate levels were significantly lower while urinary calcium excretion was significantly greater in stone formers than in controls. Thus calciuresis could be correlated with the degree of metabolic acidosis but not with the rate of urinary ammonium excretion.

摘要

为研究代谢性酸中毒时高钙尿症的机制,对68例结石患者和50例对照者进行了氯化铵负荷(长时间)试验。结石患者和对照者服用氯化铵后,尿量、铵和钙排泄量均显著增加,血浆钙和肌酐清除率无变化,血浆碳酸氢盐显著降低。然而,在氯化铵负荷试验的第三天,结石患者的尿铵排泄量和血浆碳酸氢盐水平显著低于对照者,而尿钙排泄量显著高于对照者。因此,钙利尿可能与代谢性酸中毒的程度相关,而与尿铵排泄率无关。

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