Effect of dietary salt intake on circadian calcium metabolism, bone turnover, and calcium oxalate kidney stone risk in postmenopausal women

Increasing dietary salt (sodium chloride) increases urinary calcium excretion, which may increase the risk of developing osteoporosis and kidney stones. Ten postmenopausal women without osteoporosis or kidney stones who were not undergoing hormone replacement therapy ate all meals in a metabolic unit for 14 days: 7 days at each salt level in a crossover design. The 2 diets differed only by the addition of 150-mmol salt supplement to a 50-mmol baseline diet containing 780-mg calcium. Urinary calcium was higher in all 10 subjects taking the high-salt diet. Fasting calcitriol was not different. Comparing fasting with mid-morning, mid-afternoon, and evening samplings on day 7 of each diet, urinary deoxypyridinoline and N-telopeptide concentrations per mmol creatinine were higher in the evening on the high-salt diet. Fasting and postdinner osteocalcin values were higher on the low-salt diet. Ionized calcium, mid-molecule parathyroid hormone, and bone alkaline phosphatase were not different at any time point. Urinary volume, calcium, and oxalate but not magnesium, citrate, and the calculated calcium oxalate kidney stone risk index were higher on the high-salt diet. High dietary salt intakes by non-stone-forming postmenopausal women not taking estrogen may increase the risk of developing osteoporosis but not that of calcium oxalate kidney stones.