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Kidney stones affect 12% of the American population.
They can be extremely painful and expensive to treat. 50% of
people treated for a kidney stone will have a recurrence within
10 years. Calcium oxalate stones account for 90% of kidney
stone incidence. The majority of these calcium-containing kidney
stones are associated with unexplained hypercalciuria (elevated
calcium in the urine), although diseases such as hyperparathyroidism,
sarcoidosis and some cancers can contribute to stone formation.
Since 20-40% of recurrent stones are associated with elevated urinary calcium,
it has been thought that consumption of high levels of calcium might cause
or contribute to stone formation. In the past, it was not uncommon for patients
with renal stones who also have hypercalciuria to have their intake of calcium
sharply restricted. Medical science has shown, however, that stones can be
prevented successfully without restricting calcium intake, provided that
a number of other measures are also followed. Moreover, there is some evidence
that calcium restriction may actually increase the risk of kidney stones
under certain conditions.
Calcium Intake
and Stone Prevention
The largest prospective epidemiological study ever published on calcium and
kidney stones, (New England Journal of Medicine, 1993),
concluded that high calcium intake is associated with a decreased
risk of symptomatic kidney stones(1). Perhaps just as importantly,
the study, conducted among over 45,000 men, found that those
individuals who consumed less than
850 mg of calcium per day were at an incresed risk for a higher incidence of kidney stones.
The authors concluded that calcium may actually have a protective effect
by binding to oxalate in the gut and preventing its absorption in a form
that leads to kidney stones. In another study calcium restriction led to an increase in absorption
and excretion of oxalate in the urine in both normal subjects and patients
with kidney stones. The authors, as well as many previous investigators,
have also concluded that urinary oxalate appears to be more important than
urinary calcium in the formation of stones.
This conclusion was supported by a subsequent study on long-term calcium
supplementation in premenopausal women which found no increase in stone formation(2).
Calcium supplementation lowered both urinary oxalate and urinary phosphorous
(also thought to contribute to the formation of stones) by binding both agents
in the intestine.
Other Dietary
Factors Contributing to Stones
If
high calcium intake is not the major factor contributing
to increased risk of kidney stones, what is? The study
published in the New England Journal
of Medicine in 1993 found that higher consumption of animal protein was associated
with increased stone formation and that higher fluid intake was associated
with decreased stone formation.
Another study examining 282 patients with a history of confirmed calcium
oxalate kidney stones searched for hypercalciuria (excess calcium in the
urine) often associated with stones(3). A large number of patients who were
hypercalciuric on their normal diets decreased their urinary calcium excretion
when placed on a controlled high-calcium diet. Something other than calcium
intake, most likely sodium, was causing the high urinary calcium, and perhaps
the kidney stones.
Salt, Calcium
Excretion and Stones
Sodium intake has turned out to be important
in creating excess urinary excretion of calcium. In a critical review "Dietary
Salt, Urinary Calcium, and Kidney Stone Risk" the authors found stone
formers may be more sensitive to salt intake than non-stone formers and that
a reduced intake of salt may decrease the risk of kidney stone formation(4).
Additionally, high sodium intake has been associated with urinary
calcium losses contributing to postmenopausal osteoporosis and
bone loss, particularly for those with a low calcium intake.
This study showed that sodium may also be responsible for the
high urinary calcium seen in kidney stone patients. Sodium was
as important, or more important, than dietary calcium in determining
how much calcium was excreted in stone forming patients.
Oxalate and
Kidney Stones
In a review
of studies of dietary oxalate, the authors found that a
decrease in dietary calcium intake led to greater urinary
oxalate(5). Since less calcium was available to bind the
oxalate into a non-absorbable form in the stomach and intestines,
more oxalate was absorbed and then excreted through the
urine, raising the risk for kidney stones.
This review also identified eight specific oxalate-containing foods that
significantly increase urinary oxalate, and therefore the potential for calcium-oxalate
stones. These foods included nuts, tea, chocolate, beets, rhubarb and wheat bran. This finding suggests a strategy of limiting intake of certain
very high oxalate-containing foods in people prone to calcium oxalate stone
formation, and maintaining adequate calcium intake.
Finally, phosphate-based soft drinks have been proposed as a contributor
to kidney stones. A study in the Journal of Clinical Epidemiology reviewed
1,009 male patients who both formed kidney stones and were consumers of a
significant amount of soda to see what effect soda might have on stone
recurrence(6). Those people who consumed phosphate-based sodas in the largest
quantities had the highest rate of stone recurrence.
Osteoporosis
Risk and Kidney Stones
The
risks of following a low-calcium diet in patients with
kidney stones were reinforced in a study of low bone
mass in stone forming individuals(7). Patients with calcium containing kidney
stones, both with and without hypercalciuria, were compared with normal subjects
for bone mineral density and incidence of bone fractures.
As a group, stone forming patients had lower bone density than non-stone
formers. However, when correlated with diet, those kidney stone patients
with lower bone density and more fractures consumed a diet with less calcium
and more salt and animal protein than those with better bone quality and
fewer fractures.
Calcium Intake
and Kidney Stones: Risk Benefit
While the NIH Consensus Development
Conference on Optimal Calcium Intake cautioned those patients with a history
of kidney stones and high urinary calcium about increasing their calcium
intake excessively, the report also cited the study published in the New England Journal of Medicine in 1993 showing a protective
effect of higher calcium intake in reducing the risk of kidney stones(8).
Most recently, the authors of the 1993 prospective
study, published further data on calcium intake and stones(9).
In this latest study, the authors conducted an analysis among
women participating in the Nurses Health Study over a 12-year
period who had no prior history of kidney stones. They found
that higher dietary calcium intake was correlated with fewer
kidney stones.
Although those subjects taking calcium supplements had a slightly higher
risk of stones, the incidence was only I case of stones per 1,000 person
years. The authors propose that since 67% of women taking calcium supplements
took them between meals or with breakfast, a meal usually low in oxalate,
the calcium could not perform its role of blocking oxalate stone formation
the same way that calcium at meals is able to do. Supplemental calcium may reduce kidney stone risk especially if taken
with meals.
In the recently completed Calcium for Preclampsia Prevention trial, only
two cases of kidney stones were reported in 2,295 pregnant women taking 2,000
mg of supplemental calcium carbonate per day(10).
Conclusion
The best strategy for preventing kidney stones and maintaining healthy bones
would appear to be adequate calcium consumption from the diet and supplements
taken at mealtime if necessary, combined with restriction of sodium, oxalate-rich
foods and phosphate-based sodas in people at risk for stones. Most importantly,
a high fluid intake should be maintained at all times, especially during
hot, dry weather when the risk of kidney stone formation is greatest.
Calcium carbonate achieves maximum absorption when taken with meals, and
therefore is an excellent choice as a supplement. It is also the most widely
used supplement, contains the highest amount of elemental calcium of all
supplements and is moderately priced.
References:
- (1) Curhan, G.C. et al., "A Prospective Study
of Dietary Calcium and Other Nutrients and the Risk
of
Symptomatic Kidney Stones," New England Journal
of Medicine, 328:833838, 1993.
- (2) Sakhaee, K. et al., "Limited Risk of Kidney
Stone Formation During Long-Term Calcium Citrate
Supplementation in Nonstone Forming Subjects," Journal of
Urology,
152:324-327, 1994.
- (3) Burtis, William J. et al., "Dietary Hypercalciuria
inn Patients with Calcium Oxalate Kidney Stones," American
Journal of Clinical Nutrition, 60:424-429, 1994.
- (4) Massey, L.K., and S.J. Whiting, "Dietary
Salt, Urinary Calcium, and Kidney Stone Risk," Nutrition
Reviews, 53:131-139, 1995.
- (5) Massey, Linda K., et al., "Effect of Dietary
Oxalate and Calcium on Urinary Oxalate and Risk of
Formation of Calcium Oxalate Kidney Stones, " Journal
of the American Dietetic Association, 93:901-906,
1993.
- (6) Shuster, J. et al., "Soft Drink Consumption
and Urinary Stone Recurrence: A Randomized Prevention
Trial," Journal of Clinical Epidemiology,
45-911-916, 1992.
- (7) Jaeger, P. et al., "Low Bone Mass in Idiopathic
Renal Stone Formers: Magnitude and Significance," Journal
of Bone and Mineral Research, 9:1525, 1994.
- (8) "Optimal Calcium Intake," NIH Consensus
Development Panel on Optimal Calcium Intake, Journal
of the American Medical Association, 272:1942-1948,
1994.
- (9) Curhan, G.C., et al., "Comparison of Dietary
Calcium with Supplemental Calcium and Other Nutrients
as Factors Affecting the Risk for Kidney Stones in
Women," Annals of Internal Medicine,
126:497-504, 1997.
- (10) Levine, R.I. and CPEP Study Group (NICHD), "Calcium
for Preeclampsia Prevention (CPEP): A Double-Blind,
Placebo-Controlled Trial in Healthy Nulliparas," SPO
Abstract, 1997.
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