LIMITED RISK OF KIDNEY-STONE FORMATION DURING LONG-TERM CALCIUM CITRATE SUPPLEMENTATION IN NONSTONE FORMING SUBJECTS

Citation
K. Sakhaee et al., LIMITED RISK OF KIDNEY-STONE FORMATION DURING LONG-TERM CALCIUM CITRATE SUPPLEMENTATION IN NONSTONE FORMING SUBJECTS, The Journal of urology, 152(2), 1994, pp. 324-327
Citations number
19
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00225347
Volume
152
Issue
2
Year of publication
1994
Part
1
Pages
324 - 327
Database
ISI
SICI code
0022-5347(1994)152:2<324:LROKFD>2.0.ZU;2-0
Abstract
The physiological and physicochemical effects of long-term calcium cit rate supplementation (25 mmol. calcium per day) were assessed in 7 nor mal premenopausal women. Calcium citrate increased urinary calcium fro m 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). A fter 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 t han the pretreatment value (p <0.0125). Fractional intestinal calcium absorption and serum 1,25-dihydroxyvitamin D levels decreased marginal ly at 1 month of calcium citrate therapy, from 0.457 +/- 0.092 to 0.37 4 +/- 0.035 (p <0.05) and from 103 +/- 7 to 77 +/- 14 pmol./l. (p <0.0 5), respectively. After 3 months of treatment fractional intestinal ca lcium absorption decreased further to 0.341 +/- 0.061 (p <0.0125 compa red to pretreatment), whereas serum 1,25-dihydroxyvitamin D remained u nchanged at 82 +/- 14 pmol./l. Calcium citrate treatment decreased uri nary 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. Urinar y saturation of calcium oxalate and brushite did not change during cal cium citrate therapy, except at 1 month when the saturation of calcium oxalate increased marginally. The inhibitory activity of urine agains t spontaneous nucleation of calcium oxalate and brushite (formation pr oduct) did not change during treatment. In conclusion, long-term calci um citrate supplementation in normal subjects does not increase the pr opensity for crystallization of calcium salts in the urine. This prote ctive effect is probably due to the attenuated increase in urinary cal cium excretion (from a decrease in fractional intestinal calcium absor ption), a decrease in urinary phosphorus and an increase in urinary ci trate.