Sutton R A, Mavichak V, Halabe A, Wilkins G E
Department of Medicine, University of British Columbia, Vancouver, Canada.
Miner Electrolyte Metab. 1992;18(1):43-51.
Renal tubular function was examined in 5 adult patients aged 18-30 years with Bartter's syndrome associated with renal magnesium wasting and hypocalciuria. In the 3 patients studied during hypotonic saline diuresis, distal tubular fractional chloride reabsorption was lower than that reported in normal subjects. In response to a single intravenous dose of furosemide (40 mg), the increment in the excretion of sodium, chloride, and magnesium was equal to or greater than in normal subjects, while in 2 patients, in response to intravenous chlorothiazide (500 mg), the increment in sodium excretion was less than in normal subjects. Magnesium chloride infusion was undertaken in 2 patients in order to compare magnesium and calcium excretions at similar plasma magnesium levels in patients and in normal subjects. The patients exhibited magnesium wasting only at normal or low plasma magnesium levels, while calcium excretion was reduced in the patients at normal and elevated plasma magnesium levels. We conclude that in these patients the enhancement of renal magnesium reabsorption by hypomagnesemia is defective, and the hypomagnesemia is not the cause of the hypocalciuria. The tubule defect responsible for these abnormalities of magnesium and calcium excretion may be located beyond the side of action of furosemide, in the thiazide-sensitive segment of the distal convoluted tubule.
对5名年龄在18至30岁之间、患有与肾镁消耗和低钙尿症相关的巴特综合征的成年患者进行了肾小管功能检查。在3名处于低渗盐水利尿期接受研究的患者中，远端肾小管氯化物重吸收分数低于正常受试者报告的数值。静脉注射单次剂量速尿（40毫克）后，钠、氯和镁的排泄增量等于或大于正常受试者，而在2名患者中，静脉注射氯噻嗪（500毫克）后，钠排泄增量低于正常受试者。对2名患者进行了氯化镁输注，以便比较患者和正常受试者在相似血浆镁水平下的镁和钙排泄情况。患者仅在正常或低血浆镁水平时出现镁消耗，而在正常和升高血浆镁水平时患者的钙排泄均减少。我们得出结论，在这些患者中，低镁血症增强肾镁重吸收的功能存在缺陷，且低镁血症不是低钙尿症的原因。导致镁和钙排泄出现这些异常的肾小管缺陷可能位于速尿作用部位之外，即在远曲小管的噻嗪敏感段。
