TY - JOUR
T1 - Physicochemical action of potassium‐magnesium citrate in nephrolithiasis
AU - Pak, Charles Y C
AU - Koenig, Karl
AU - Khan, Rubina
AU - Haynes, Sharon
AU - Padalino, Paulette
PY - 1992/3
Y1 - 1992/3
N2 - Effect of potassium‐magnesium citrate on urinary biochemistry and crystallization of stone‐forming salts was compared with that of potassium citrate at same dose of potassium in five normal subjects and five patients with calcium nephrolithiasis. Compared to the placebo phase, urinary pH rose significantly from 6.06 ± 0.27 to 6.48 ± 0.36 (mean ± SD, p < 0.0167) during treatment with potassium citrate (50 mEq/day for 7 days) and to 6.68 ± 0.31 during therapy with potassium‐magnesium citrate (containing 49 mEq K, 24.5 mEq Mg, and 73.5 mEq citrate per day). Urinary pH was significantly higher during potassium‐magnesium citrate than during potassium citrate therapy. Thus, the amount of undissociated uric acid declined from 118 ± 61 mg/day during the placebo plase to 68 ± 54 mg/day during potassium citrate treatment and, more prominently, to 41 ± 46 mg/day during potassium‐magnesium citrate therapy. Urinary magnesium rose significantly from 102 ± 25 to 146 ± 37 mg/day during potassium‐magnesium citrate therapy but not during potassium citrate therapy. Urinary citrate rose more prominently during potassium‐magnesium citrate therapy (to 1027 ± 478 mg/day from 638 ± 252 mg/day) than during potassium citrate treatment (to 932 ± 297 mg/day). Consequently, urinary saturation (activity product) of calcium oxalate declined significantly (from 1.49 × 10−8 to 1.03 × 10−8 M2) during potassium‐magnesium citrate therapy and marginally (to 1.14 × 10−8 M2) during potassium citrate therapy. Moreover, the formation product of calcium phosphate (brushite), indicative of inhibition against spontaneous nucleation, rose more prominently during potassium‐magnesium citrate treatment (from 4.62 × 10−7 to 8.78 × 10−7 M2) than during potassium citrate therapy (to 6.08 × 10−7 M2). The inhibition against agglomeration of calcium oxalate increased marginally (p = 0.02) during potassium‐magnesium citrate therapy, whereas it did not change significantly during potassium citrate treatment. Thus, potassium‐magnesium citrate (at same dose of potassium) is more effective than potassium citrate in inhibiting the crystallization of uric acid and calcium oxalate in urine.
AB - Effect of potassium‐magnesium citrate on urinary biochemistry and crystallization of stone‐forming salts was compared with that of potassium citrate at same dose of potassium in five normal subjects and five patients with calcium nephrolithiasis. Compared to the placebo phase, urinary pH rose significantly from 6.06 ± 0.27 to 6.48 ± 0.36 (mean ± SD, p < 0.0167) during treatment with potassium citrate (50 mEq/day for 7 days) and to 6.68 ± 0.31 during therapy with potassium‐magnesium citrate (containing 49 mEq K, 24.5 mEq Mg, and 73.5 mEq citrate per day). Urinary pH was significantly higher during potassium‐magnesium citrate than during potassium citrate therapy. Thus, the amount of undissociated uric acid declined from 118 ± 61 mg/day during the placebo plase to 68 ± 54 mg/day during potassium citrate treatment and, more prominently, to 41 ± 46 mg/day during potassium‐magnesium citrate therapy. Urinary magnesium rose significantly from 102 ± 25 to 146 ± 37 mg/day during potassium‐magnesium citrate therapy but not during potassium citrate therapy. Urinary citrate rose more prominently during potassium‐magnesium citrate therapy (to 1027 ± 478 mg/day from 638 ± 252 mg/day) than during potassium citrate treatment (to 932 ± 297 mg/day). Consequently, urinary saturation (activity product) of calcium oxalate declined significantly (from 1.49 × 10−8 to 1.03 × 10−8 M2) during potassium‐magnesium citrate therapy and marginally (to 1.14 × 10−8 M2) during potassium citrate therapy. Moreover, the formation product of calcium phosphate (brushite), indicative of inhibition against spontaneous nucleation, rose more prominently during potassium‐magnesium citrate treatment (from 4.62 × 10−7 to 8.78 × 10−7 M2) than during potassium citrate therapy (to 6.08 × 10−7 M2). The inhibition against agglomeration of calcium oxalate increased marginally (p = 0.02) during potassium‐magnesium citrate therapy, whereas it did not change significantly during potassium citrate treatment. Thus, potassium‐magnesium citrate (at same dose of potassium) is more effective than potassium citrate in inhibiting the crystallization of uric acid and calcium oxalate in urine.
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U2 - 10.1002/jbmr.5650070306
DO - 10.1002/jbmr.5650070306
M3 - Article
C2 - 1585829
AN - SCOPUS:0026554159
SN - 0884-0431
VL - 7
SP - 281
EP - 285
JO - Journal of Bone and Mineral Research
JF - Journal of Bone and Mineral Research
IS - 3
ER -