The Role of Diet in the Prevention
Of Common Kidney Stones
Christy Krieg
Kidney stone formers may
feel doomed to a life of
unpredictable flank pain,periodic surgical intervention,
and concomitant loss of
work and daily pleasures. Indeed,
if untreated, those who have
formed one calcium oxalate stone
have a 50% chance of forming
additional stones within 10 years
(Menon & Resnick, 2002). With
appropriate education, patients
can exercise some control over
stone disease and reduce their
chances of forming stones
through dietary modifications
and medication.
General dietary recommendations
appropriate for patients
who form the most common
metabolic stone types — calcium
oxalate and uric acid — will be discussed
in this article. Patients with
a tendency to form cystine and
brushite stones may also benefit
from some of the same dietary recommendations,
but dietary management
is a small part of an even
more complex treatment regimen
in these instances. Regardless of
stone type, recommendations for
dietary modifications are most
accurate when tailored to the
results of urine stone risk profiles,
or “24-hour urine” studies.
These studies typically provide
total urine volume, urine
calcium, sodium, citrate and uric
Current dietary recommendations for patients who form kidney
stones are discussed. Focusing on the most common kidney stone
types, calcium oxalate and uric acid, the rationale for dietary changes
are described based on the renal and urine physiology.
Christy Krieg, BSN, RN, is a Clinical
Nurse, Methodist Urology, Indianapolis,
IN.
Note: CE Objectives and Evaluation
Form appear on page 457.
acid, as well as pH, and supersaturation
of critical compounds,
among other measurements. The
values, if properly interpreted,
allow the clinician to observe the
patient’s specific abnormalities,
recommend medication and/or
dietary modification, and track
progress through followup studies.
As with many bodily
processes, stone formation is a
complicated and multi-factorial
process. Yet, there is much still to
be understood about stone formation.
For example, we know that
stone formation runs in families,
but while all humans form calcium
oxalate crystals, most do not
form stones (Lemann, 2002). And
while for years calcium stone formers
were instructed to restrict
dietary calcium, there is now significant
evidence against this recommendation
(Borghi et al.,
2002). These observations illustrate
the sometimes counterintuitive
and always complex nature
of stone formation and the need
for ongoing investigation.
Stone recurrence is frustrating
for patients who have made
changes in their lives and yet still
form stones. While diet alone
cannot always control the disease,
dietary measures can
absolutely help supplement
other therapies, and for some
patients are the primary tool for
stone prevention. As a component
of the medical management
for stone disease, the goal of therapy
should be to improve those
factors thought to contribute to
stone formation in the urinary
tract, and thereby reduce the
chance of forming stones, even if
the disease is not eliminated.
Urine Supersaturation
And Stone Formation
Urine volume plays a pivotal
role in the process of stone formation.
In particular, low volume,
highly concentrated urine
contributes to the supersaturation
of elements normally found
in the urine, such as calcium
oxalate. Simply put, when the
solute exceeds the solvent’s ability
to dissolve it, precipitation of
crystals can occur. Consider an
attempt to dissolve sugar in
water: a tablespoon of sugar is
readily dissolved in a glass of
water, but eight tablespoons of
sugar in that same glass will not
completely dissolve, resulting in
the accumulation of crystals in
the bottom of the glass. In this
scenario, the water is saturated
with sugar; the solvent, water,
can dissolve no more solute. It
has exceeded the point of saturation,
and is supersaturated.
Fortunately, urine has the
unique quality of holding more
solute in suspension than does
water and so can accept large
concentrations of solute without
precipitation. The ability of urine
to keep such large concentrations
in solution is, in part, due to the
presence of protective organic
molecules like citrate, as well as
the presence of charged ions
which alter the solubility (Menon
& Resnick, 2002). Despite the fact
that calcium oxalate can be present
in urine in concentrations 7
to 11 times its solubility in water
(Menon & Resnick, 2002), the
point exists at which calcium
oxalate exceeds the unique properties
of urine; crystals will then
form and possibly aggregate to
form stones.
Understanding saturation principles
in the urine, is it not clear
that methods of prevention shall be
focused on both an increase in solvent
and a reduction of solute?
These two concepts are the basis
for the dietary changes described
below.
Assessment of Dietary
Patterns
As dietary history is not part
of the typical urologic patient
history forms, the nurse can
obtain this information through
patient interview. Important information
includes the patient’s
intake of fluids throughout the
day, environmental factors promoting
dehydration, special diets
such as now-popular high-protein
diets, and a propensity to
consume packaged or restaurant
foods which are typically very
high in sodium. What does the
patient drink, how much is consumed,
and how is fluid intake
distributed through the day?
Does he or she work in a hot or
dry environment (such as a hot
factory, outside work in the summer)?
Does he or she prepare
fresh foods at home or tend to eat
convenience foods?
Nurses’ dietary interview can
occur before or after metabolic
testing. Absent metabolic testing,
this interview has even greater
import as it is the only source of
information about dietary habits.
Asking patients to keep a 24-hour
diet record may help identify
patterns of which even the
patient was unaware. Sources of
dietary sodium can be obvious or
insidious. The excess intake of a
patient who consumes a bag of
microwave popcorn every night
is more apparent than the intake
of a patient who drinks sports
drinks after a daily workout;
these are both very high in sodium,
but the latter is less often
recognized.
If the nurse has at his or her
disposal a 24-hour urine study,
dietary anomalies may be more
specifically exposed and documented.
This author views 24-
hour urine studies as “vice recognition
software;” the numbers
show actual urine output, and
indicate dietary sodium, protein,
and oxalate excess. Patients with
low urine volumes may believe
their results are incorrect. They
may say “I drink all the time!”
and yet the output is low. Here
the role of dietary counseling is
critical; the insightful nurse
helps the patient identify volume
consumed, sources of insensible
loss, and ways to ensure
increased urine volume.
DIETARY CHANGES TO
PREVENT AND REDUCE
STONE FORMATION
Increase Fluid Intake
Increasing urine volume can
reduce supersaturation, and is
widely known to help prevent
stone formation. Recommendations
for urinary output vary, but there is
general agreement that it should
exceed two liters per day, while
some even encourage urinary
outputs in excess of three liters
per day (Menon & Resnick, 2002;
Sakhaee, Zerwekh, & Pak, 1980).
A key point is that the dilution of
urine is necessary “24/7,” or all
day, every day. A patient who
voids the recommended two
liters a day between the hours of
8 am and 10 pm, but only 300
milliliters during the remaining
10 hours of the day will have saturated
urine overnight, with the
possibility of precipitation and
aggregation during the sleeping
hours. Patients must accept the
necessity of getting up at least
twice at night to urinate, and
should consume more water each
time they rise to void.
Stress to patients that it is not
the quantity of fluid consumed
that is important, but rather the
fluid voided that should be measured.
Patients living in hot or
dry conditions, or who exercise
and perspire significantly, will
need to drink even more liquid to
maintain adequate urine output.
Many patients ask what fluids
are recommended, and which
are prohibited. The simple
answer is that water is best. For
those with excessive urinary
oxalates, black tea should be
eliminated because black tea is a
high-oxalate beverage. Curhan,
Willett, Rimm, Speizer, and
Stampfer (1998) found, in a retrospective
study of previously nonstone
forming women from the
Nurses’ Health Study, that the
type of beverages consumed
proved relevant for stone formers.
Of the 17 beverages studied,
and after correcting for other contributing
factors, those who
drank one daily 8 ounce glass of
grapefruit juice had a 44%
increased risk of a stone event in
the 8-year period, while the risk
was decreased by 8% to 10% for
each daily 8 ounce serving of coffee
(both caffeinated and non-caffeinated),
tea, or wine. A prospective study had similar
conclusions for men, additionally
showing that beer had a protective
effect and apple juice increased
the risk of stone events (Curhan,
Willett, Rimm, Speigelman, &
Stampfer, 1996). Also, a study published
by Massey and Sutton (2004)
showed a modest positive relationship
between caffeine intake and
urinary calcium levels in stone formers
and non-stone formers, so caffeinated
beverages should be limited
in stone formers. In summary,
stone formers should drink more
water and avoid excess caffeine,
black tea, and grapefruit and apple
juices.
What do these studies mean
for patient education?
Water is the
best beverage for stone formers. It is
non-caloric, non-caffeinated, and
contains insignificant amounts of
solutes. In initial attempts to
increase patients’ fluid intake, it
may be appropriate to advise them
to drink whatever they can consume
in large quantities. However,
warning them of side effects of sugared
and caffeinated beverages in
large quantities is important. The
results discussed above indicate
that consumption of alcoholic
beverages is unlikely to increase
stone risk. Water that tastes good
(filtered, reverse osmosis, bottled)
may be easier to consume than tap
water, so encourage patients to
seek a source of good-tasting
water. There is no clear agreement
on the impact of drinking water’s
mineral content on lithogenesis;
“hard water” may not be problematic
for most patients (Menon &
Resnick, 2002). Again, water in
large quantities should be the
focus of prevention. Lemonade is
often recommended, as it supplies
dietary citrate, a stone inhibitor
and pH buffer when excreted later
in the urine.
Encourage patients to set
consumption goals, carry water
with them at all times, and strive
for pale urine throughout the day
and night. Some patients describe
an initial physiologic
resistance to increased fluid
intake which eases as their bodies
and minds learn the new
habit of extra fluid intake and
output. According to Parks,
Goldfischer, and Coe (2003),
aims by clinicians to increase
patients’ urinary volumes often
fall short, and follow-up metabolic
studies showed an average
increase in urine output of only
0.3 liters per 24 hours. This
increase was associated with a
curious increase in sodium
intake. High urine volumes
should be the goal of all patients
who form stones. In this
instance, more is definitely better.
Most patients find that after
forcing fluids for a couple of
months, their bodies crave fluids
and their habit is to drink more.
Consume Adequate Calcium
High urine calcium, hypercalciuria,
is associated both with
formation of kidney stones and
with osteoporosis. Sufficient calcium
intake is required for the
growth and maintenance of the
skeleton in children and adults.
Reducing urine calcium should
be a goal for stone formers, but
not via dietary restriction. While
reduced dietary calcium can
decrease urine calcium (Lemann,
2002), calcium restriction is no
longer advisable for patients who
form calcium kidney stones as
this puts them at risk of bone disease,
namely osteoporosis. Recall
that bones are in a constant
process of resorption and formation;
adequate calcium is required
for the ongoing rebuilding of bone
material.
Several recent studies have
shown, in fact, that adequate calcium
intake is associated with
decreased stone formation.
Curhan, Willett, Knight, and
Stampfer (2004) found that in
previously non-stone forming
younger women, higher intake of
dietary calcium was related to
lower risk of kidney stone formation.
Additionally, a 5-year randomized
clinical trial of men
with a history of calcium oxalate
stones found that a normal calcium,
decreased sodium, and
decreased animal protein diet
was more effective for reducing
stone events than was a restricted
calcium diet (Borghi et al., 2002).
So, adequate calcium plus
decreased sodium and protein
intake had a significantly more
protective effect against stones
than decreased calcium intake
alone.
Why might increased dietary
calcium reduce the risk of calcium
stone formation? Calcium
and oxalate bind in the gut and
in the urine to form a nonabsorbable
compound. Low dietary
calcium permits greater free
oxalate to be absorbed in the gut
and excreted in the urine, which
may be counterproductive for
calcium oxalate stone formers.
Restricted calcium intake results
in increased urinary oxalates, a
risk for stone formation (Menon
& Resnick, 2002). This is a proposed
cause of the association
between reduced calcium intake
and increased supersaturation of
calcium oxalate (Lemann, 2002).
Clearly, strong research evidence
now supports adequate
calcium intake for patients who
form kidney stones. Low-fat
dairy products, green leafy vegetables,
broccoli, fortified foods,
and almonds are excellent
sources. Patients should consume
enough dietary calcium to
meet (but not exceed) the United
States Recommended Daily
Allowance (RDA) of calcium,
which ranges from 1,000 to 1,200
milligrams daily for adults. The
recommendations are the same
for men and women, but vary by
age group (see Table 1). Patients
should avoid calcium supplements
in favor of calcium-rich
foods; a patient with intolerance
to dairy products may supplement,
but should not exceed the
RDA for his/her age group.
Limit Dietary Oxalates
Oxalate is found in many
foods, but there is considerable
variability in the amount, which
depends upon where the food is
grown. Likewise, individual
absorption of oxalate also varies,
which makes adequate calcium
intake critically important.
Nonetheless, oxalate restriction
should be attempted. The highest
levels of oxalate are found in
chocolate, nuts, beans (including
soybeans), rhubarb, spinach,
beets, and black tea. A thorough
oxalate list can be found on the
Web site of the Oxalosis and
Hyperoxaluria Foundation (http://
www.ohf.org/diet.html). This list
is exhaustive and may be overwhelming
to patients. Stress that
reduction of high oxalate foods is
the goal for typical stone formers
rather than strict avoidance of all
oxalate-containing foods (which
would be very difficult). Followup
24-hour urine studies will demonstrate
the adequacy of patients’
restriction.
Though only 10% to 20% of
urinary oxalates come from
dietary sources (Morton, Iliescu,
& Wilson, 2002), dietary reduction
is commonly advised for calcium
oxalate stone formers. It has
been suggested that because
there is much less oxalate in the
urine than calcium in the urine,
urinary oxalate concentration is
much more critical to the formation
of calcium oxalate crystals
than is the urinary calcium concentration;
reducing urine oxalates
may have a more powerful effect
on stone formation than can reduction
of urine calcium (Morton et
al., 2002). Patients with calcium
oxalate stones, particularly those
with documented hyperoxaluria,
should avoid foods high in
oxalates. Vitamin C is a precursor
to endogenous production of
oxalates, so some clinicians recommend
avoiding mega-doses of
vitamin C. The rare genetic condition
of primary hyperoxaluria is
only slightly impacted by dietary
reduction, and causes serious
medical problems besides kidney
stones.
Limit Sodium Intake
Because calcium and sodium
compete for reabsorption in the
renal tubules, excess sodium
intake and consequent excretion
result in loss of calcium in the
urine. High-sodium diets are
associated with greater calcium
excretion in the urine (Lemann,
2002). Metabolic studies often
reveal exceptionally high urine
calcium over 24 hours, related to
patients’ exceptionally high sodium
excretion. Patients may deny
salt intake, stating, “I never salt
my food!” They quite likely are
ignorant of hidden sodium
sources in the diet. Sodium is a
common preservative in canned
and frozen foods, and is endemic
in restaurant foods. Instruction
on careful inspection of food
labels and wise food choices
helps patients identify and
reduce sodium in their diets.
A notable dietary “ah-ha!”
was the admission by one patient
that, on the day of 24-hour urine
testing, she ate a full jar of pickles
to reduce stress, and then
drank the brine; needless to say,
her urine sodium was very high
on the day of her stress mitigation.
The role of the nurse or dietician
in shedding light on sources
of sodium cannot be underestimated.
Repeated, persistent inquiry
into dietary habits may be necessary.
The goal of therapy should be
a “no added salt diet,” or the equivalent
of 2,000 mg per day or less of
dietary sodium. Reduction of
dietary sodium is difficult and disappointing
to patients. They may
believe they have made significant
reductions and sacrifices, while
their urine sodium remains high.
Consultation with a registered
dietician may help the patient
achieve the specific goal of a sodium
intake of 2,000 milligrams or
less per day.
Limit Animal Protein
The effect of excess animal
protein (purine) is most obvious
for the uric acid stone former.
Uric acid, a byproduct of purine
metabolism, is excreted in large
quantities in the urine. Excess
protein creates urine with high
total urine uric acid, potentially
high supersaturation of urine
uric acid, and a low pH, necessary
for formation of uric acid
stones. There is no inhibitor of
uric acid crystal formation
(Menon & Resnick, 2002), so
dietary measures focus on reducing
uric acid and increasing
urine volume. Reduction of animal
protein to 12 ounces per day
for adults is recommended. This
is plenty to meet the dietary
needs of most Americans, many
of whom typically consume several
more ounces of animal protein
daily than is recommended.
Protein from plant sources
(beans, legumes, etc.) can be substituted
as a dietary alternative
without negative consequences.
Calcium oxalate stone formers
reducing their animal protein
should note the oxalate content
of substitute proteins.
The role of excess protein in
promoting calcium stone formation
is less obvious, but equally
important. High dietary protein
is associated with increased urinary
calcium. Thus, there is a
link between meat consumption
and both uric acid and calcium
stone formation. In fact, vegetarians
form stones at one-third the
rate of those eating a mixed diet
(Lemann, 2002). A study of 18
hypercalciuric stone formers found
that a 15-day protein restriction
had many positive effects on urinary
markers of stone risk.
Namely, significant decreases
were seen in urine calcium, urine
uric acid, urine phosphate, and
urine oxalate. And, for unclear
reasons, a beneficial increase in
urinary citrate was observed
(Giannini et al., 1999). Citrate is a
known inhibitor of calcium
oxalate crystal formation and
also increases pH, which can prevent
uric acid stones. Clearly, the
benefits of protein restriction for
stone formers are many.
Weight Loss
A relationship between weight,
body mass index and risk of calcium
oxalate stone formation was
established in a retrospective
study of health professionals.
Curhan and colleagues (1998)
found that “the prevalence of
stone disease history and the
incidence of stone disease were
directly associated with weight
and body mass index. However,
the magnitude of the associations
was consistently greater among
women” (p. 1645). The value of
weight loss for stone prevention
has not been proven, but given
the benefits of weight loss for
general health, it is certainly
worth mentioning to overweight
patients who form stones.
Educational Resources
There are excellent resources
on the Internet for patients seeking
nutritional information. One stellar
example is NutritionData
(www.nutritiondata.com/). Here
patients can search by general food
category, like “pickle,” to view the
standard sodium content, as well
as a plethora of additional information
regarding vitamin and mineral
content, calories, suggested healthier
substitutes, and even the individual
amino acid compositions of
each protein. The site also provides
detailed information about
thousands of specific brand items
from grocery and fast food restaurants.
Under “Tools,” patients can
search within food categories like
“dairy products” for choices highest
in calcium and lowest in sodium.
This site is complex and may be
overwhelming to patients without
good computer and Web skills, but
is extraordinarily comprehensive;
unfortunately, this site does not list
oxalate content. For that purpose,
refer patients to www.ohf.org.
For patients without Web
access, nurses might find it helpful
to review a general nutrition
book for charts and diagrams to
help patients understand nutrition
content. Show patients a
sample food label from a can of
soup so they know where to find
sodium content on foods at home.
For a simple list of high-oxalate
foods, visit www.gicare.com/
pated/edtgs29.htm.
Conclusion
The dietary measures discussed
have value particularly
for patients who form the most
common types of kidney stones:
calcium oxalate and uric acid.
That said, they may be insufficient
to control the various metabolic
abnormalities present in
individual patients. The most
effective management of kidney
stones includes in-depth metabolic
studies, recommendations
tailored to patients regarding
medications and dietary changes,
and follow-up to ensure changes
are having the desired effect.
Urine studies should be repeated
to judge progress approximately
6 to 8 weeks after initial metabolic
testing recommendations are
implemented. Once a stable state
is reached in which the patient’s
urine demonstrates decreased
risk of stone formation, metabolic
testing should be performed
(along with an x-ray to check for
stone growth) at least annually to
monitor stone risk. The cycle of
stone formation can be altered,
and in some cases broken, with
the aid of effective dietary management.
Every patient need not make
all of these changes to his/her
diet, but in the absence of
patient-specific urine studies,
none of these recommendations
is harmful. Aside from oxalate
consumption, the dietary recommendations
for calcium oxalate
and uric acid stone formers are
the same. Assessing
patients’ dietary habits can shed
light on potential areas of
improvement. For example, a
receptive uric acid stone former
on a high-protein diet for weight
loss could benefit from counseling
on the effects of this diet on
his/her stone disease.
Of course, talking about
dietary changes is easier than actual
implementation. Encourage
patients to make changes at a realistic
pace. Praise even modest
progress and stress the value of
striving for improvement rather
than perfection.
The Bottom Line here is;
•Urinate more than two liters per day.
• Consume enough dietary calcium to meet the US RDA.
• Avoid dietary oxalates (for calcium oxalate stone-formers).
• Limit sodium to 2,000 milligrams per day.
• Limit protein to 12 ounces per day.
• If overweight, lose weight.
