Ruml L A, Pak C Y
Center for Mineral Metabolism and Clinical Research, Northwest Jersey Medical Associates, Dallas, PA, USA.
Am J Kidney Dis. 1999 Jul;34(1):107-13. doi: 10.1016/s0272-6386(99)70115-0.
The study was performed to ascertain the value of potassium magnesium citrate, magnesium citrate, and potassium citrate in overcoming thiazide-induced hypokalemia and magnesium loss. Sixty-two healthy subjects were first administered hydrochlorothiazide, 50 mg/d. After 3 weeks of thiazide treatment (or earlier for potassium level </=3.5 mEq/L), they were randomized to receive one of three drugs while continuing to receive thiazide: potassium magnesium citrate (49 mEq of potassium, 24.5 mEq of magnesium), magnesium citrate (24.5 mEq/d of magnesium), or potassium citrate (49 mEq/d of potassium). Outcome measures were changes in serum potassium and magnesium levels and urinary potassium, magnesium, pH, and citrate values. All three drugs increased serum potassium concentration compared with that resulting from thiazide alone. Potassium magnesium citrate increased serum potassium levels from 3.3 +/- 0.2 to 3.8 +/- 0.3 mEq/L (P < 0.001), potassium citrate increased serum potassium levels from 3.4 +/- 0.4 to 3.9 +/-0.3 mEq/L (P < 0.001), and magnesium citrate from 3.4 +/- 0.4 to 3.7 +/- 0.3 mEq/L (P < 0.001). Potassium magnesium citrate led to a significant increase in urinary magnesium levels by the third week of supplementation (from 120 +/- 34 to 149 +/- 58 mg/d; P < 0.01) and produced a small but significant increase in serum magnesium level. Magnesium citrate significantly increased 24-hour urinary magnesium after the first week of supplementation and maintained this increase throughout the study. Potassium magnesium citrate and potassium citrate, but not magnesium citrate, significantly increased urinary pH and citrate values. Potassium magnesium citrate not only corrects thiazide-induced hypokalemia, but also may avert magnesium loss while providing an alkali load.
本研究旨在确定枸橼酸钾镁、枸橼酸镁和枸橼酸钾在克服噻嗪类药物引起的低钾血症和镁流失方面的价值。62名健康受试者首先接受每日50mg氢氯噻嗪治疗。在噻嗪类药物治疗3周后(或血钾水平≤3.5mEq/L时更早),他们被随机分配接受三种药物之一,同时继续接受噻嗪类药物治疗:枸橼酸钾镁(含49mEq钾、24.5mEq镁)、枸橼酸镁(每日24.5mEq镁)或枸橼酸钾(每日49mEq钾)。观察指标为血清钾和镁水平以及尿钾、镁、pH值和枸橼酸盐值的变化。与单独使用噻嗪类药物相比,所有三种药物均提高了血清钾浓度。枸橼酸钾镁使血清钾水平从3.3±0.2mEq/L升至3.8±0.3mEq/L(P<0.001),枸橼酸钾使血清钾水平从3.4±0.4mEq/L升至3.9±0.3mEq/L(P<0.001),枸橼酸镁使血清钾水平从3.4±0.4mEq/L升至3.7±0.3mEq/L(P<0.001)。补充枸橼酸钾镁至第三周时,尿镁水平显著升高(从120±34mg/d升至149±58mg/d;P<0.01),血清镁水平有小幅但显著的升高。补充枸橼酸镁第一周后,24小时尿镁显著增加,并在整个研究过程中维持这一增加。枸橼酸钾镁和枸橼酸钾可显著提高尿pH值和枸橼酸盐值,但枸橼酸镁无此作用。枸橼酸钾镁不仅能纠正噻嗪类药物引起的低钾血症,还可能在提供碱负荷的同时避免镁流失。