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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
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