UROLOGICAL SURVEY   ( Download pdf )

 

STONE DISEASE

Effect of dietary calcium on stone forming propensity
Heller HJ, Doerner MF, Brinkley LJ, Adams-Huet B, Pak CY
Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-8885, USA
J Urol. 2003; 169:470-4

  • Purpose: Epidemiological studies have reported that high calcium diet protects against kidney stone formation in normal subjects. This metabolic study was designed to elucidate the physiological and physicochemical effects conferring this apparent protection.
  • Materials and Methods: A total of 21 normal volunteers underwent 2 phases of study in a crossover, randomized design, wherein they consumed constant metabolic diets that matched the estimated highest and lowest quintiles of calcium intake from published epidemiological studies.
  • Results: Urinary calcium was significantly greater on the high calcium diet (148 +/- 55 versus 118 +/- 43 mg. daily, p <0.01, p <0.01) but urinary oxalate did not differ between diets. There was no difference in relative saturation ratio of calcium oxalate between the 2 diets. The high calcium diet significantly increased saturation of brushite and decreased that of uric acid. Due to the other differences between the diets (more fluid, potassium, magnesium and phosphate in the high calcium diet), the high calcium diet also increased 24-hour urinary volume, potassium, phosphorus, pH and citrate. After adjustment of these confounding variables, the high calcium diet significantly increased relative saturation ratio of calcium oxalate by 24%.
  • Conclusions: High calcium diet from published epidemiological studies does not alter the propensity for calcium oxalate crystallization in normal subjects despite increased urinary calcium and unaltered urinary oxalate because of the greater amounts of ingested fluid, potassium and phosphate. However, high calcium intake alone, without concomitant changes in the diet, poses a modest risk for calcium stone formation.

  • Editorial Comment
    The role of dietary calcium in stone formation is controversial. Although high urinary calcium has been implicated in calcium stone disease, no prospective randomized trial has definitively established a link between urinary calcium and stone disease. Indeed, a recent long-term prospective, randomized trial demonstrated a higher incidence of stone formation in a group of hypercalciuric stone formers maintained on a low calcium diet compared with a similar group taking a normal calcium, low protein, low sodium diet. Likewise, 2 large populational studies showed a higher rate of incident stone formation in subjects in the highest quintile of calcium intake compared with the lowest. In both cases, the protective effect of a high calcium diet was attributed to reduced urinary oxalate as a result of intestinal binding of oxalate by calcium, which reduces intestinal oxalate absorption and decreases urinary oxalate excretion.
    Heller and colleagues attempted to reproduce the high and low calcium diets from the observational studies by Curhan and colleagues in order to assess the physiological and physicochemical responses to changes in dietary calcium. In this 2-phase, randomized crossover study, 21 normal subjects were maintained on a constant metabolic diet matched to the dietary compositions of the highest and lowest quintiles of calcium intake in the epidemiological studies. Not surprisingly, urinary calcium was higher on the high calcium diet; however urinary oxalate and the relative saturation ratio for calcium oxalate were not significantly different between groups as a result of other stone-protective factors in the high calcium diet such as higher fluid, potassium and magnesium, which resulted in increased urinary volume, citrate and pH. Controlling for these confounding factors, the high calcium diet in fact increased the relative saturation ratio of calcium oxalate.
    Based on this study, the “protective effect” of a high calcium diet may well not reside not in lowering of urinary oxalate but rather in the other favorable factors associated with a high calcium diet such as high fluid intake and an alkali load. Indeed urinary calcium increases significantly with a high calcium diet. As oxalate intake was fairly limited in this study, no increase in urinary oxalate was seen with the low calcium diet as had been speculated in the previous studies. However, with a more liberal oxalate intake, urinary oxalate could potentially increase in response to a low calcium diet. Nonetheless, indiscriminate recommendations to increase calcium intake in stone formers based on the findings of these recent studies may in fact pose additional risk of stone formation if concomitant measures, such as increased fluid and alkali intake are not taken.

Dr. Margaret S. Pearle
Associate Professor of Urology
University of Texas Southwestern Med Ctr
Dallas, Texas, USA