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High Urinary Calcium Excretion and Genetic Susceptibility to Hypertension and Kidney Stone Disease

Andrew Mente^*, R. John D’ A. Honey, John M. McLaughlin^*, Shelley B. Bull^* and Alexander G. Logan^*

^* Prosserman Centre for Health Research, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, and Department of Public Health Sciences; and St. Michael’s Hospital, Division of Urology, Department of Surgery, University of Toronto, Toronto, Ontario, Canada

Address correspondence to: Dr. Alexander G. Logan, Department of Medicine, Division of Nephrology, Mount Sinai Hospital, Room 435, 600 University Avenue, Toronto, Ont M5G1X5, Canada. Phone: 416-586-5187; Fax: 416-586-8434; alogan{at}mtsinai.on.ca

Received for publication December 22, 2005. Accepted for publication June 8, 2006.

Increased urinary calcium excretion commonly is found in patients with hypertension and kidney stone disease (KSD). This study investigated the aggregation of hypertension and KSD in families of patients with KSD and hypercalciuria and explored whether obesity, excessive weight gain, and diabetes, commonly related conditions, also aggregate in these families. Consecutive patients with KSD, aged 18 to 50 yr, were recruited from a population-based Kidney Stone Center, and a 24-h urine sample was collected. The first-degree relatives of eligible patients (n = 333) and their spouse were interviewed by telephone to collect demographic and health information. Familial aggregation was assessed using generalized estimating equations. Multivariate-adjusted odds ratios (OR) revealed significant associations between hypercalciuria in patients and hypertension (OR 2.9; 95% confidence interval 1.4 to 6.2) and KSD (OR 1.9; 95% confidence interval 1.03 to 3.5) in first-degree relatives, specifically in siblings. No significant associations were found in parents or spouses or in patients with hyperuricosuria. Similarly, no aggregation with other conditions was observed. In an independent study of siblings of hypercalciuric patients with KSD, the adjusted mean fasting urinary calcium/creatinine ratio was significantly higher in the hypertensive siblings compared with normotensive siblings (0.60 ± 0.32 versus 0.46 ± 0.28 mmol/mmol; P < 0.05), and both sibling groups had significantly higher values than the unselected study participants (P < 0.001). Urinary sodium/creatinine and uric acid/creatinine ratios were not different among the groups. Although an environmental effect cannot be excluded fully, our findings suggest that the disturbance in calcium metabolism in hypertension and KSD has a genetic basis.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673