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    Dietary Calcium and Kidney Stones

    Kidney stones are a significant problem in the United States. Kidney stones will develop in approximately 10% of men and 3% of women at some time during their adult lives. Direct costs for managing kidney stone patients is in excess of $2 billion annually, and costs are rising as medical costs in general rise, and also because the incidence of kidney stones is rising. Since the majority of stones (80% to 85%) contain calcium oxalate, alone or with a nucleus of calcium phosphate, and since a substantial number of patients (some 20% to 40%) with recurrent kidney stones have hypercalciuria, patients are advised to reduce dietary calcium intake, even those who do not have hypercalciuria. Yet case-control studies have not demonstrated any difference in mean calcium intake between patients with kidney stones and controls, nor have there been any good studies showing that calcium restriction alters the rate of stone recurrence.

    Recently Curhan et al. reported the results of their carefully conducted epidemiologic study of the effects of dietary calcium on the prevalence of kidney stones in a cohort of 45,619 men enrolled in the Health Professionals Follow-up Study (HPFS). The HPFS is a longitudinal study of cardiovascular disease and cancer in 51,529 male dentists, optometrists, osteopaths, pharmacists, podiatrists, and veterinarians. At the time of enrollment in 1986, participants were 40 - 75 years of age; at the time of the study after 4 years of follow-up, those with a history of kidney stones (4357 men) were excluded from the analysis. The investigators used data from questionnaires -- a comprehensive medical/dietary questionnaire in 1986, plus follow-up questionnaires -- to determine calcium intake, then assessed the reproducibility and validity of the dietary questionnaire by carefully studying 127 of the participants (all foods and drinks were weighed and recorded during two one-week periods 6 to 8 months apart). The mean daily intake of calcium based on dietary records was 796 mg, which closely corresponds to the 804 mg/day calculated from questionnaires. During 165,090 person-years of follow-up, there were 505 documented cases of new symptomatic kidney stones, most commonly in men aged 40 - 59. A family history of kidney stones (through first cousins) was reported by about 26%.

    Analysis of the data yielded some very interesting results. The incidence of kidney stones during follow-up was almost 50% lower among the men with the highest energy-adjusted calcium intake (mean 1326 mg per day) than in the men whose intake was lowest (516 mg per day). Not only do these results provide no support for the contention that higher dietary calcium intake increases the risk of symptomatic kidney stones, the data actually suggest that the relationship may be inverse. The relative risk for men in the highest quintile of calcium intake was 0.56 compared with the lowest quintile, and this risk remained significant (0.66) after adjustment for age, profession, thiazide use, and the intakes of animal protein, potassium, or alcohol. Further adjustment for geographic region, physical activity, body-mass index, and intake of sodium, vitamin D, phosphorus, coffee, sucrose, and sugared cola did not alter the results. There was no significant interaction between calcium intake and other variables. An examination of the daily calcium sources showed that skim or low-fat milk and cottage cheese or ricotta cheese had the strongest inverse relation with risk. Men who drank two or more eight-ounce glasses of skim milk per day had close to half the incidence (risk 0.58) of men who drank less than one glass per month. Other calcium-rich foods that appeared to be protective were yogurt, oranges, and broccoli. A retrospective analysis of the 4357 men in whom kidney stones developed found the same inverse association between calcium intake and stone formation.

    As with other studies, animal protein intake was found to be directly associated with the risk of kidney stones, while potassium intake and fluid intake were inversely related to risk. Relative risks for men in the highest as compared with the lowest quintile were 1.33 for animal protein intake, 0.49 for potassium intake, and 0.71 for fluid intake. Animal-protein intake increases the excretion of uric acid and calcium and lowers urinary citrate excretion, all of which predispose to stone formation (calcium citrate, a highly soluble calcium salt, decreases free calcium in the urine). Potassium supplementation reduces calcium excretion, while increased fluid intake dilutes the urine. Sodium, magnesium, phosphorus, sucrose, fiber, and sugared cola were not associated with risk, and adjusting for these nutrients did not materially alter the protective effect of dietary calcium. Thiazide diuretics reduced the risk; after controlling for potential confounders, the relative risk for men taking a thiazide diuretic was 0.55. The mean daily intake of animal protein, magnesium, vitamin D, phosphorus, potassium, and total fluid increased with increasing dietary calcium intake, while mean daily alcohol intake decreased with increasing calcium intake. Mean daily sodium intake was similar in all quintiles, as were the percentages of men who took calcium supplements or a thiazide diuretic.

    "These prospective data provide no support for the belief that higher consumption of calcium from dietary sources increases the risk of symptomatic kidney stones," said Curhan et al, "in fact, the data suggest that the relation may actually be inverse." Although questionnaires are often unreliable, "any misclassification would be random with respect to case statusE and hence would result in an underestimation of the protective effect of calcium."

    So how does calcium protect against kidney stones? The investigators suggest that urinary oxalate may be more important in stone formation than urinary calcium. Even small increases in urinary oxalate concentration rapidly boost the calcium oxalate saturation of urine, thus promoting crystal growth. Urinary oxalate concentration is reduced when oxalate is excreted via the feces rather than in the urine, and fecal excretion is promoted by calcium binding oxalate in the intestines, thus reducing absorption. Calcium restriction is known to increase the absorption of oxalate in the gastrointestinal tract of normal subjects as well as patients with kidney stones, leading to a substantial (16% to 56%) increase in urinary oxalate excretion. Thus dietary calcium restriction could actually be harmful by increasing the excretion of oxalate via the urine. Increasing dietary calcium intake, on the other hand, has been shown to reduce urinary oxalate excretion. According to editorialist Jacob Lemann, urinary oxalate excretion falls by 1.1 to 1.8 mg (0.01 to 0.02 mmol) per day for every increase of 100 mg per day of dietary calcium intake. Thus high dietary calcium intake could substantially reduce calcium oxalate saturation of the urine. (Lemann J. N Engl J Med 1993; 328: 880 - 881.)

    Oxalate is found in small quantities in many foods; however, Curhan et al. did not find an association between the risk of kidney stones and the consumption of foods relatively high in oxalate (chocolate, tea, nuts, and spinach). Calcium supplements given with oxalate decrease urinary oxalate excretion, but supplements taken without food (which is more often the case) may increase calcium absorption and urinary calcium excretion and thus risk. This would explain Curhan's observation that calcium supplements did not have the apparent protective effect of dietary calcium, probably because of the timing of the dose. While the Curhan study involved men 40 years of age and older with no history of kidney stones, the investigators feel there is no reason to believe their results wouldn't hold true for women, younger men, and men with a history of kidney stones. "The general policy of calcium restriction for patients who have had kidney stones containing calcium should be reexamined."


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