Limited risk of kidney stone formation during long-term calcium citrate supplementation in nonstone forming subjects

K. Sakhaee, S. Baker, J. Zerwekh, J. Poindexter, P. A. Garcia-Hernandez, C. Y C Pak

Research output: Contribution to journalArticle

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Abstract

The physiological and physicochemical effects of long-term calcium citrate supplementation (25 mmol. calcium per day) were assessed in 7 normal premenopausal women. Calcium citrate increased urinary calcium from 3.27 ± 0.42 mmol. per day (standard deviation) before treatment to 5.16 ± 0.75 mmol. per day after 1-month of treatment (p <0.0125). After 3 months of treatment urinary calcium decreased from the 1-month value to 4.54 ± 0.67 mmol. per day (p <0.0125) but remained higher than the pretreatment value (p <0.0125). Fractional intestinal calcium absorption and serum 1,25- dihydroxyvitamin D levels decreased marginally at 1 month of calcium citrate therapy, from 0.457 ± 0.092 to 0.374 ± 0.035 (p <0.05) and from 103 ± 7 to 77 ± 14 pmol./l. (p <0.05), respectively. After 3 months of treatment fractional intestinal calcium absorption decreased further to 0.341 ± 0.061 (p <0.0125 compared to pretreatment), whereas serum 1,25-dihydroxyvitamin D remained unchanged at 82 ± 14 pmol./l. Calcium citrate treatment decreased urinary phosphorus levels significantly from 18.9 ± 3.3 to 15.0 ± 2.5 mmol. per day (p <0.0125) and 14.0 ± 2.5 mmol. per day (p <0.05) at 1 and 3 months, respectively. Mean urinary oxalate decreased by 15 to 20% and urinary citrate increased marginally during treatment. Urinary saturation of calcium oxalate and brushite did not change during calcium citrate therapy, except at 1 month when the saturation of calcium oxalate increased marginally. The inhibitory activity of urine against spontaneous nucleation of calcium oxalate and brushite (formation product) did not change during treatment. In conclusion, long-term calcium citrate supplementation in normal subjects does not increase the propensity for crystallization of calcium salts in the urine. This protective effect is probably due to the attenuated increase in urinary calcium excretion (from a decrease in fractional intestinal calcium absorption), a decrease in urinary phosphorus and an increase in urinary citrate.

Original languageEnglish (US)
Pages (from-to)324-327
Number of pages4
JournalJournal of Urology
Volume152
Issue number2
StatePublished - 1994

Fingerprint

Calcium Citrate
Kidney Calculi
Calcium
Calcium Oxalate
Intestinal Absorption
Therapeutics
Citric Acid
Phosphorus
Urine
Oxalates
Crystallization
Serum
Salts

Keywords

  • calcium dietary
  • citrates
  • kidney calculi
  • urinary calculi

ASJC Scopus subject areas

  • Urology

Cite this

Limited risk of kidney stone formation during long-term calcium citrate supplementation in nonstone forming subjects. / Sakhaee, K.; Baker, S.; Zerwekh, J.; Poindexter, J.; Garcia-Hernandez, P. A.; Pak, C. Y C.

In: Journal of Urology, Vol. 152, No. 2, 1994, p. 324-327.

Research output: Contribution to journalArticle

Sakhaee, K. ; Baker, S. ; Zerwekh, J. ; Poindexter, J. ; Garcia-Hernandez, P. A. ; Pak, C. Y C. / Limited risk of kidney stone formation during long-term calcium citrate supplementation in nonstone forming subjects. In: Journal of Urology. 1994 ; Vol. 152, No. 2. pp. 324-327.
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abstract = "The physiological and physicochemical effects of long-term calcium citrate supplementation (25 mmol. calcium per day) were assessed in 7 normal premenopausal women. Calcium citrate increased urinary calcium from 3.27 ± 0.42 mmol. per day (standard deviation) before treatment to 5.16 ± 0.75 mmol. per day after 1-month of treatment (p <0.0125). After 3 months of treatment urinary calcium decreased from the 1-month value to 4.54 ± 0.67 mmol. per day (p <0.0125) but remained higher than the pretreatment value (p <0.0125). Fractional intestinal calcium absorption and serum 1,25- dihydroxyvitamin D levels decreased marginally at 1 month of calcium citrate therapy, from 0.457 ± 0.092 to 0.374 ± 0.035 (p <0.05) and from 103 ± 7 to 77 ± 14 pmol./l. (p <0.05), respectively. After 3 months of treatment fractional intestinal calcium absorption decreased further to 0.341 ± 0.061 (p <0.0125 compared to pretreatment), whereas serum 1,25-dihydroxyvitamin D remained unchanged at 82 ± 14 pmol./l. Calcium citrate treatment decreased urinary phosphorus levels significantly from 18.9 ± 3.3 to 15.0 ± 2.5 mmol. per day (p <0.0125) and 14.0 ± 2.5 mmol. per day (p <0.05) at 1 and 3 months, respectively. Mean urinary oxalate decreased by 15 to 20{\%} and urinary citrate increased marginally during treatment. Urinary saturation of calcium oxalate and brushite did not change during calcium citrate therapy, except at 1 month when the saturation of calcium oxalate increased marginally. The inhibitory activity of urine against spontaneous nucleation of calcium oxalate and brushite (formation product) did not change during treatment. In conclusion, long-term calcium citrate supplementation in normal subjects does not increase the propensity for crystallization of calcium salts in the urine. This protective effect is probably due to the attenuated increase in urinary calcium excretion (from a decrease in fractional intestinal calcium absorption), a decrease in urinary phosphorus and an increase in urinary citrate.",
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N2 - The physiological and physicochemical effects of long-term calcium citrate supplementation (25 mmol. calcium per day) were assessed in 7 normal premenopausal women. Calcium citrate increased urinary calcium from 3.27 ± 0.42 mmol. per day (standard deviation) before treatment to 5.16 ± 0.75 mmol. per day after 1-month of treatment (p <0.0125). After 3 months of treatment urinary calcium decreased from the 1-month value to 4.54 ± 0.67 mmol. per day (p <0.0125) but remained higher than the pretreatment value (p <0.0125). Fractional intestinal calcium absorption and serum 1,25- dihydroxyvitamin D levels decreased marginally at 1 month of calcium citrate therapy, from 0.457 ± 0.092 to 0.374 ± 0.035 (p <0.05) and from 103 ± 7 to 77 ± 14 pmol./l. (p <0.05), respectively. After 3 months of treatment fractional intestinal calcium absorption decreased further to 0.341 ± 0.061 (p <0.0125 compared to pretreatment), whereas serum 1,25-dihydroxyvitamin D remained unchanged at 82 ± 14 pmol./l. Calcium citrate treatment decreased urinary phosphorus levels significantly from 18.9 ± 3.3 to 15.0 ± 2.5 mmol. per day (p <0.0125) and 14.0 ± 2.5 mmol. per day (p <0.05) at 1 and 3 months, respectively. Mean urinary oxalate decreased by 15 to 20% and urinary citrate increased marginally during treatment. Urinary saturation of calcium oxalate and brushite did not change during calcium citrate therapy, except at 1 month when the saturation of calcium oxalate increased marginally. The inhibitory activity of urine against spontaneous nucleation of calcium oxalate and brushite (formation product) did not change during treatment. In conclusion, long-term calcium citrate supplementation in normal subjects does not increase the propensity for crystallization of calcium salts in the urine. This protective effect is probably due to the attenuated increase in urinary calcium excretion (from a decrease in fractional intestinal calcium absorption), a decrease in urinary phosphorus and an increase in urinary citrate.

AB - The physiological and physicochemical effects of long-term calcium citrate supplementation (25 mmol. calcium per day) were assessed in 7 normal premenopausal women. Calcium citrate increased urinary calcium from 3.27 ± 0.42 mmol. per day (standard deviation) before treatment to 5.16 ± 0.75 mmol. per day after 1-month of treatment (p <0.0125). After 3 months of treatment urinary calcium decreased from the 1-month value to 4.54 ± 0.67 mmol. per day (p <0.0125) but remained higher than the pretreatment value (p <0.0125). Fractional intestinal calcium absorption and serum 1,25- dihydroxyvitamin D levels decreased marginally at 1 month of calcium citrate therapy, from 0.457 ± 0.092 to 0.374 ± 0.035 (p <0.05) and from 103 ± 7 to 77 ± 14 pmol./l. (p <0.05), respectively. After 3 months of treatment fractional intestinal calcium absorption decreased further to 0.341 ± 0.061 (p <0.0125 compared to pretreatment), whereas serum 1,25-dihydroxyvitamin D remained unchanged at 82 ± 14 pmol./l. Calcium citrate treatment decreased urinary phosphorus levels significantly from 18.9 ± 3.3 to 15.0 ± 2.5 mmol. per day (p <0.0125) and 14.0 ± 2.5 mmol. per day (p <0.05) at 1 and 3 months, respectively. Mean urinary oxalate decreased by 15 to 20% and urinary citrate increased marginally during treatment. Urinary saturation of calcium oxalate and brushite did not change during calcium citrate therapy, except at 1 month when the saturation of calcium oxalate increased marginally. The inhibitory activity of urine against spontaneous nucleation of calcium oxalate and brushite (formation product) did not change during treatment. In conclusion, long-term calcium citrate supplementation in normal subjects does not increase the propensity for crystallization of calcium salts in the urine. This protective effect is probably due to the attenuated increase in urinary calcium excretion (from a decrease in fractional intestinal calcium absorption), a decrease in urinary phosphorus and an increase in urinary citrate.

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