Physicochemical action of potassium-magnesium citrate in nephrolithiasis

Charles Y C Pak, Karl Koenig, Rubina Khan, Sharon Haynes, Paulette Padalino

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)281-285
Number of pages5
JournalJournal of Bone and Mineral Research
Volume7
Issue number3
StatePublished - Mar 1992

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Nephrolithiasis
Potassium Citrate
Therapeutics
Calcium Oxalate
potassium-magnesium citrate
Crystallization
Uric Acid
Citric Acid
Potassium
Placebos

ASJC Scopus subject areas

  • Surgery

Cite this

Physicochemical action of potassium-magnesium citrate in nephrolithiasis. / Pak, Charles Y C; Koenig, Karl; Khan, Rubina; Haynes, Sharon; Padalino, Paulette.

In: Journal of Bone and Mineral Research, Vol. 7, No. 3, 03.1992, p. 281-285.

Research output: Contribution to journalArticle

Pak, CYC, Koenig, K, Khan, R, Haynes, S & Padalino, P 1992, 'Physicochemical action of potassium-magnesium citrate in nephrolithiasis', Journal of Bone and Mineral Research, vol. 7, no. 3, pp. 281-285.
Pak, Charles Y C ; Koenig, Karl ; Khan, Rubina ; Haynes, Sharon ; Padalino, Paulette. / Physicochemical action of potassium-magnesium citrate in nephrolithiasis. In: Journal of Bone and Mineral Research. 1992 ; Vol. 7, No. 3. pp. 281-285.
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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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