Vitamin D deficiency may be linked to stone formation
November 1, 2010
Findings from a small observational study suggest a role of vitamin D deficiency in so-called "idiopathic" hypercalciuria and support the need for further research investigating an association between vitamin D deficiency and renal stone formation.
The relationship between vitamin D deficiency and hypercalciuria was also examined in a separate study in which vitamin D repletion was not found to increase the risk of hypercalciuria in patients with vitamin D deficiency.
"These data suggest that patients with elevated PTH levels and normal serum calcium may have vitamin D deficiency leading to increased calcium excretion, and they support conducting prospective trials to investigate the effects of vitamin D repletion as a means to correct hypercalciuria and prevent stone formation," said Dr. Pareek, who is also director of minimally invasive urologic surgery at Alpert Medical School.
Such a study is now being planned as a collaborative project between the Alpert Medical School urologists and Brian H. Eisner, MD, and colleagues at Massachusetts General Hospital, Boston.
At the same session at the AUA annual meeting in San Francisco, Dr. Eisner reported the results from a randomized controlled trial undertaken to evaluate the effects of vitamin D repletion in premenopausal women.
The study included 88 premenopausal women ages 18 to 45 years who were vitamin D deficient (serum 25-OHD <20 ng/mL) and had no history of stone disease. The patients were randomized to receive either placebo or vitamin D, 50,000 IU per week for a total of 12 weeks, and all women also received calcium, 1,000 to 1,500 mg/day either through dietary intake or supplementation. Mean baseline serum 25-OHD was similar in the treatment and control groups: 14.3 and 14.7 ng/mL, respectively.
No rise in urine calcium:creatinine ratio
At the end of the study, serum 25-OHD had increased significantly from baseline in both groups, but the change was slight in the placebo-treated women (final mean, 17.7 ng/mL), while there was a threefold increase in the patients receiving vitamin D supplementation (final mean, 45.8 ng/mL). Neither group had a significant change in the spot urine calcium:creatinine ratio, and results of an age-adjusted, multivariate linear regression analysis found that vitamin D repletion was not associated with an increase in the spot urine calcium:creatinine ratio.
"As vitamin D is known to increase intestinal calcium absorption, vitamin D supplementation could theoretically affect urine calcium excretion and the risk of calcium nephrolithiasis," explained Dr. Eisner, instructor in surgery at Massachusetts General Hospital.
"Based on our study, vitamin D repletion appears not to increase urine calcium levels. However, while the findings may be durable, the study was relatively short term and assessed possible changes in urinary excretion levels based on spot collections. Further research should include 24-hour urine collection for better quantification of the effects of vitamin D repletion and must assess the possible impact of longer-term vitamin D treatment.
Dr. Pareek observed that vitamin D deficiency is a hot topic now in medicine, with particular interest in its role in malignancies along with a variety of other disease states. As such, an increasing number of patients are presenting with results from measurement of their serum vitamin D level.
At Alpert Medical School and at Massachusetts General Hospital, the metabolic stone evaluation protocol was recently modified to include measurement of serum 25-OHD. However, Dr. Pareek acknowledged that the cost-effectiveness of such routine testing and the clinical relevance of the data are yet to be determined.