The study was performed to ascertain the value of potassium magnesium citra
te, magnesium citrate, and potassium citrate in overcoming thiazide-induced
hypokalemia and magnesium loss. Sixty-two healthy subjects were first admi
nistered hydrochlorothiazide, 50 mg/d. After 3 weeks of thiazide treatment
(or earlier for potassium level less than or equal to 3.5 mEq/L), they were
randomized to receive one of three drugs while continuing to receive thiaz
ide: potassium magnesium citrate (49 mEq of potassium, 24.5 mEq of magnesiu
m), magnesium citrate (24.5 mEq/d of magnesium), or potassium citrate (49 m
Eq/d of potassium). Outcome measures were changes in serum potassium and ma
gnesium levels and urinary potassium, magnesium, pH, and citrate values. Al
l three drugs increased serum potassium concentration compared with that re
sulting from thiazide alone. Potassium magnesium citrate increased serum po
tassium 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 m
Eq/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 i
n 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 in
crease in serum magnesium level. Magnesium citrate significantly increased
24-hour urinary magnesium after the first week of supplementation and maint
ained this increase throughout the study. Potassium magnesium citrate and p
otassium citrate, but not magnesium citrate, significantly increased urinar
y pH and citrate values. Potassium magnesium citrate not only corrects thia
zide-induced hypokalemia, but also may avert magnesium loss while providing
an alkali load. (C) 1999 by the National Kidney Foundation, Inc.