Risk of calcium oxalate nephrolithiasis after calcium or combined calcium and calcitriol supplementation in postmenopausal women

Citation
S. Domrongkitchaiporn et al., Risk of calcium oxalate nephrolithiasis after calcium or combined calcium and calcitriol supplementation in postmenopausal women, OSTEOPOR IN, 11(6), 2000, pp. 486-492
Citations number
36
Categorie Soggetti
Endocrynology, Metabolism & Nutrition
Journal title
OSTEOPOROSIS INTERNATIONAL
ISSN journal
0937941X → ACNP
Volume
11
Issue
6
Year of publication
2000
Pages
486 - 492
Database
ISI
SICI code
0937-941X(2000)11:6<486:ROCONA>2.0.ZU;2-Z
Abstract
Although calcium supplementation can cause hypercalciuria, the risk of neph rolithiasis has been shown to decrease rather than increase among subjects who had a higher calcium intake. Hypercalciuria is also a well-established side effect of calcitriol administration. However, the risk of nephrolithia sis is not well defined. The present study was undertaken to prospectively determine the effect of calcium with or without calcitriol on physicochemic al risk factors associated with calcium oxalate nephrolithiasis in Thai pos tmenopausal women with osteoporosis. Subjects consisted of 53 Thai women mo re than 10 years postmenopausal who were randomly allocated to receive 750 mg of calcium carbonate supplement alone (n = 28) or 750 mg of calcium carb onate plus 0.5 mu g calcitriol (n = 25) daily. Mean+/-SEM for age was 65.3 +/- 1.1 years, body weight 53.5 +/- 1.3 kg. Urine samples for biochemical a ssays were collected at baseline and 3 months after treatment. Supersaturat ion for calcium oxalate stone formation was assessed from the 24 h urine co nstituents by the Tiselius's index, AP(CaOx). Three months of calcium suppl ement alone resulted in a modest, but not significant, increase in urinary calcium (baseline, 2.90+/-0.33 mmol/day; after treatment 3.58 +/- 0.54 mmol /day) with no change in urinary oxalate, citrate or magnesium. In contrast, calcium together with calcitriol caused a significant increase in urinary calcium (baseline, 2.87+/-0.41 mmol/day; after treatment, 4.08 +/- 0.57 mmo l/day; p < 0.05). No significant change in other urine constituents after t reatment with calcium and calcitriol was detected. Therefore, AP(CaOx) did not significantly increase either after calcium alone (baseline, 1.17+/-0.3 9; after treatment, 1.36+/-0.28) or after calcium plus calcitriol (baseline , 1.09+/-0.17; after treatment, 1.09+/-0.19). However, after treatments, 12 subjects (23%)- 6 receiving calcium supplement alone and 6 receiving calci um plus calcitriol supplement - had high AP(CaOx) values (greater than the upper limit of 95% CI for AP(CaOx) derived from non-stone-forming Thai wome n). The post-treatment/baseline ratio was 3.21+/-0.74 for urinary calcium, 1.01+/-0.19 for urinary oxalate, and 2.23+/-0.42 (median 1.15) for AP(CaOx) . The post-treatment/baseline ratio of calcium, but not for urinary oxalate , had a significant correlation with the post-treatment/baseline ratio of A P(CaOx). Our findings suggest that the alteration in the risk of calcium ox alate nephrolithiasis based on urinary composition is related to the altera tion ill urinary calcium. The risk of calcium oxalate nephrolithiasis does not increase significantly after calcium or combined calcium and calcitriol supplement in the majority of postmenopausal women with osteoporosis.