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Diet and Calcium: The End of an Era
- Fredric L. Coe, MD;
- Joan H. Parks, MBA; and
- Murray J. Favus, MD
- University of Chicago Medical School, Chicago, IL 60637 Grant Support: By a George M. O'Brien Center of Excellence Grant DK47631, from the National Institute of Diabetes and Digestive and Kidney Diseases. Requests for Reprints: Fredric L. Coe, MD, Renal Section, MC 5100, University of Chicago Medical School, 5841 South Maryland Avenue, Chicago, IL 60637. Current Author Addresses: Drs. Coe and Favus and Ms. Parks: University of Chicago Medical School, 5841 South Maryland Avenue, Chicago, IL 60637. Grant Support: By a George M. O'Brien Center of Excellence Grant DK47631, from the National Institute of Diabetes and Digestive and Kidney Diseases. Requests for Reprints: Fredric L. Coe, MD, Renal Section, MC 5100, University of Chicago Medical School, 5841 South Maryland Avenue, Chicago, IL 60637. Current Author Addresses: Drs. Coe and Favus and Ms. Parks: University of Chicago Medical School, 5841 South Maryland Avenue, Chicago, IL 60637.
Because the main constituents of most human kidney stones are calcium salts, intuition has always linked stone formation to levels of urinary calcium. The discovery by Flocks [1] of otherwise asymptomatic hypercalciuria (so-called idiopathic hypercalciuria) in a majority of stone formers made this association more compelling. Since at least 1936, idiopathic hypercalciuria has been a recognized clinical diagnosis that affects upward of 70% of patients who make calcium-containing stones [2]. Naturally, clinical belief would presume that decreasing urinary calcium levels should reduce stone formation, and this belief has translated itself into several therapeutic actions.
An abnormally efficient intestinal absorption of diet calcium is well known in idiopathic hypercalciuria [3, 4], as well as in primary hyperparathyroidism, sarcoidosis, immobilization, and vitamin D intoxication (other reasonably common hypercalciuric stone-forming states) [2]. In the case of idiopathic hypercalciuria, hyperabsorption seemed the main, perhaps the only abnormality. Low-calcium diet, therefore, offered itself as a reasonable treatment, and such diets have long enjoyed popularity [5, 6]. But a number of problems have gradually emerged and have, by this time, pushed low-calcium diets out of favor. One problem is that no prospective, controlled trials have ever shown that dietary measures are effective in stone prevention, whereas thiazide diuretics, when used as long-term therapy, do prevent stones by decreasing urinary calcium excretion [7].
A second problem is that bone mineral is abnormally labile in patients with idiopathic hypercalciuria. Compared with normal persons, patients with this condition excrete an abnormally high fraction of their absorbed dietary calcium …
