Diet and Kidney Stones – 2 CPE Hours
Good through December 2010
By James J. Kenney, PhD, RD, FACN – Posted 4/01/2002
What Diet Is Appropriate For Patients
With Nephroliathiasis?
Should Dietary Calcium Be Restricted?
Should Dietary Oxalate Be Reduced?
Should Dietary Protein Be Restricted?
Is It Necessary To Limit Salt Intake?
It Is Better to Reduce Salt and Animal Protein than
Calcium
Medical Treatment of Kidney Stones
Conclusions
References
Kidney stones (a.k.a. nephroliathiasis) are responsible for about 1 1/3 million
medical consults each year with treatment costing about $2 billion annually
in medical bills.[1] About 13% of Americans will experience
at least one occurrence of symptomatic kidney stones in their lifetime.[2] Men are about twice as likely to
form kidney stones as women. Most people who experience one episode of kidney
stones will experience another and many go on to have multiple recurrences.
Aside from the extreme pain involved in passing a kidney stone there is also
the danger of permanent damage to the kidney.
Before treating a patient with kidney stones with diet and/or pharmaceutical
agents it is important to determine the type of crystals making up the stones.
The chemical make-up of the stones is useful in determining the proper course
of treatment. Kidney stones may consist of a variety of organic and mineral
material. However, in most cases one compound will predominate. Sometimes kidney
stones are secondary to an infection. In this case treating the infection successfully
and preventing future infections should help prevent future kidney stones from
developing.
The tendency to form kidney stones is usually inherited. Most normal people
form small crystals of calcium phosphate, magnesium phosphate, uric acid, calcium
oxalate but these crystals do not grow large enough to form stones large enough
to obstruct the flow of fluid from the kidney through the ureter to the bladder.
The ureters are about 1/8 to 1/4 inch in diameter. When stones grow very large
they can stay in the renal pelvis area and set the stage for secondary kidney
infections. When smaller kidney stones pass through the ureters they can cause
severe lower back pain that may be accompanied by nausea and vomiting. Blood
in the urine can also result from passing kidney stones or from kidney infections.
It is important to note that a diet appropriate for treating one type of kidney
stone may or may not be helpful for treating other types of stones. However,
the vast majority of kidney stones consist of calcium salts and most of these
are predominantly calcium oxalate crystals. This review will concern itself
primarily with the dietary treatment and prevention of the most common type
of kidney stones. Table 1. below shows the relative frequency of various types
of kidney stones in Americans.
|
Table
1. Relative frequency of different types of kidney stones in U.S.
|
|
|
Major
Stone Type
|
% of all Stones
|
|
Calcium
Oxalate
|
>70
|
|
Triple
Phosphate
|
13
|
|
Calcium
phosphate
|
10
|
|
Cystine
|
3
|
|
Uric
Acid
|
2
|
|
Others
|
<1
|
Calcium oxalate stones are more likely to form as the amount of calcium and/or
oxalate excreted in the urine increases. Calcium oxalate is very poorly soluble
in water and tends to precipitate as the concentration of calcium and oxalic
acid increase in the kidney distillate.[3]
Most patients with calcium oxalate stones tend to absorb and excrete more calcium
in their urine than non-stone formers. It was long assumed that a diet low in
both calcium and oxalic acid rich foods coupled with increased fluid intake
was the best nutritional approach for people at high risk for calcium oxalate
stone formation.
Dehydration increases the concentration of minerals and organic materials in
the kidney distillate. Therefore, dehydration will increase the tendency for
crystals to form in the kidney distillate. The Tiselius Risk Index (TSI) was
developed as a measure of the tendency for calcium oxalate to precipitate in
the urine. The TSI increases as the concentration of calcium, oxalic acid, and
uric acid increase in the urine.
Hypercalciuria (increased calcium in the urine) is an important risk factor
for kidney formation. Many patients with kidney stones are known to have intestinal
hyperabsorption of calcium.[4]
This has led to the common recommendation of reducing dietary calcium intake
in patients with recurrent calcium-rich kidney stones. However, a low intake
of dietary calcium can lead to a negative calcium balance that would likely
increase the risk of osteoporosis in the long run.[5]
A reduction in dietary calcium will result in increased absorption of dietary
oxalic acid from the intestinal tract. This is because when calcium and oxalic
acid are present together in the intestinal tract they will form the poorly
soluble calcium oxalate salt. As a result both the calcium and oxalate are poorly
absorbed. A decrease in the absorption of oxalic acid from the intestines will
result in lower levels of oxalate excreted in the urine.[6]
So while restricting dietary calcium would reduce calcium excreted into the
kidney distillate it will also usually cause an increase the amount of oxalate
in the distillate as well. Therefore, it is not clear whether or not dietary
calcium restriction actually reduces the overall risk of forming calcium oxalate
kidney stones.
A prospective study of more than 45,000 men with a history of kidney stones,
found that those with a relatively high dietary intake of calcium (more than
1000 mg/day) actually experienced a 34% lower incidence of kidney stones compared
to those with a relatively low dietary calcium intake.[7]
It may be tempting to now recommend that those at high-risk of kidney stones
start taking calcium supplements but this may not be wise. In a 12 year long
prospective study of more than 90,000 nurses this same group of researchers
found that women who consumed more dietary calcium from food also experienced
a reduced risk of developing kidney stones. However, among women who took calcium
supplements there was actually about a 20% increased risk of developing kidney
stones.[8] It may
be that dietary calcium in whole foods usually reduces oxalate absorption but
calcium supplements may not always reduce oxalic acid absorption. Calcium supplements
that are not taken with oxalic acid rich foods would not be expected to decrease
oxalic acid absorption and excretion. However, they would increase the amount
of calcium absorbed and excreted in the urine.
It seems prudent to discourage the use of high dose calcium supplementation
in nearly all patients with recurrent kidney stones. Calcium containing antacids
should be avoided and those containing magnesium (e.g. Maalox) should be used
instead. However, there appears to be no reason to routinely discourage the
consumption of most calcium rich foods unless they are also very high in oxalic
acid. A calcium intake from foods of 800 to 1200 mg/day is probably best for
most patients with a history of calcium-rich kidney stones. In patients who
do not consume sufficient dietary calcium from foods one may be forced to weigh
the possible reduction of osteoporosis risk against a possible increased risk
of kidney stone formation from calcium supplementation. If a calcium supplement
is deemed more beneficial than risky it seems prudent to use one that contains
calcium citrate an as the citric acid may help keep the calcium oxalate crystals
from forming in the urine. Patients who are prescribed calcium supplements may
do better if the supplements are taken in a divided dose with meals. This should
reduce oxalic acid absorption. By contrast, taking a large single dose of calcium
before bed may very well increase the risk of calcium-rich kidney stones forming.
A supplement of potassium and magnesium citrate may help prevent stone formation
when calcium supplements are taken.[9]
Calcium citrate is preferable to other calcium supplements.
Oxalic acid occurs naturally in many plant foods. Spinach, rhubarb, Swiss chard,
cocoa powder, chocolate, beets, beet greens, peppers, strawberries, tea (both
black and green), okra, peanuts, pecans and wheat germ and bran contain sufficient
oxalic acid to increase urinary oxalate excretion. Increased oxalic acid in
the urine raises the TSI and presumably increases the risk of calcium oxalate-rich
kidney stones. One study showed that most of the above mentioned oxalic acid-containing
foods do significantly increase urinary oxalate excretion.[10] It seems reasonable to limit
the intake of these oxalic acid rich foods in people with recurrent calcium
oxalate kidney stones. Calcium oxalate is poorly absorbed so foods with as much
or more calcium as oxalic acid would probably have little impact on urinary
oxalate excretion. However, plant foods are not the only source of urinary oxalic
acid so even if all plant foods are avoided calcium oxalate stones may still
form. Oxalic acid can be derived from the breakdown of dietary protein as well
as from high doses of vitamin C.[11]
Vitamin C can be oxidized to oxalic acid in the human body. Large doses of
vitamin C have been shown to increase oxalic acid excretion in the urine.[12] Since there is no proven benefit to taking a large
amount of vitamin C supplements it seems prudent to discourage the use of such
supplements in patients with a personal or even a family history of calcium
oxalate kidney stones. Large doses of vitamin C can also increase the acidity
of the urine and this may increase the tendency for uric acid crystals to form.
Uric acid crystals can occasionally grow large enough to form kidney stones.
Small uric acid crystals can also serve as a base for the formation of large
calcium-rich stones.
Table 2 below lists foods with the most oxalic acid and high ratios
of oxalic acid to calcium. If calcium rich foods are consumed with these foods
it is likely that the absorption of oxalic acid from the gut would be reduced.
For example, if cocoa powder is added to skim milk to make a hot chocolate drink
it is likely that most of the oxalate in the cocoa powder would not be absorbed.
|
Table 2. Foods to Avoid for People with Recurring Kidney Stones
|
|
Food
|
Portion
|
Oxalate
(mg)
|
Calcium
(mg)*
|
|
Beet
greens, cooked
|
1/2
cup
|
916
|
82
|
|
|
Rhubarb,
stewed, no sugar
|
1/2
cup
|
860
|
52
|
|
|
Spinach,
cooked
|
1/2
cup
|
750
|
122
|
|
|
Beets,
cooked
|
1/2
cup
|
675
|
16
|
|
|
Swiss
Chard, cooked
|
1/2
cup
|
660
|
50
|
|
|
Spinach,
frozen
|
1/2
cup
|
600
|
122
|
|
|
Cocoa,
dry
|
1/3
cup
|
254
|
36
|
|
|
Okra,
cooked
|
1/2
cup
|
146
|
50
|
|
|
Sweet
potatoes, cooked
|
1/2
cup
|
141
|
14
|
|
|
Peanuts
|
1/3
cup
|
113
|
23
|
|
|
Tea
|
1
cup
|
75
|
0
|
|
|
Pecans,
halves
|
1/3
cup
|
74
|
11
|
|
|
Wheat
germ
|
1/4
cup
|
67
|
12
|
|
|
*Note:
Foods with a high oxalic acid to calcium ratio increase oxalic acid in
the urine.
|
A small amount of dietary protein can be converted to oxalic acid in the body
and excreted as such in the urine. In addition, dietary protein is known to
enhance calcium excretion in the urine.[13]
Both an increase in oxalate and calcium in the urine can result from increasing
dietary protein intake. Therefore, a greater dietary protein intake will usually
increase the TSI. As a result increased dietary protein will likely contribute
to kidney stone formation. The risk of kidney stone formation seems greater
from animal than vegetable proteins,[14] but this is still the matter of some scientific
debate. A recent study of patients with a history of kidney stones showed that
when the average dietary protein was reduced from 86.5 to 54 g/day there was
a reduction in urinary calcium excretion of nearly 50% (from 9.35 to 6.45 mmol/day).[15]
In addition to increasing urinary calcium and oxalate excretion most protein-rich
foods may also increase urinary uric acid levels. This is because most high-protein
foods (except milk) usually contain a large amount of purines that breakdown
into uric acid. Uric acid crystals account for only a small percentage of all
kidney stones formed. However, increased uric acid can also increase the risk
of calcium oxalate stone formation. Indeed, 10-20% of those with kidney stones
have high levels of uric acid in their blood and a history of gouty arthritis.[16] The higher sulfur amino acid content
of animal compared to vegetable proteins may increase calcium excretion. In
addition, excess sulfur-containing amino acids will increase a rare form of
kidney stones (containing cystine) in people with an inherited metabolic defect.
A randomized controlled trial found that a diet low in animal protein and higher
in vegetable protein significantly reduced the recurrence of kidney stones in
high-risk subjects.[17]
This is consistent with earlier research showing that a vegetarian diet was
associated with lower excretion of calcium, oxalate and uric acid in the urine.[18]
Of course, reducing animal protein alone reduces stone formation so it is unclear
whether the increase in dietary fiber itself was also protective.
A diet with more plant foods would contain more citrate, magnesium and potassium.
Many patients with calcium oxalate stones have low levels of citrate, potassium
and magnesium in their urine. This is important because citric acid is known
to reduce the tendency for calcium oxalate crystals to form. Potassium citrate
is particularly effective in reducing stone formation in patients who do not
have hypercalciuria but do have a low level of urinary citrate excretion. Urinary
citrate drops with increasing urinary acid content so a diet high in whole grains,
fruits and vegetables may be more effective than potassium citrate supplementation
alone because such a diet will reduce urine acidity and increase potassium,
magnesium, and citric acid intake.[19]
Potassium-magnesium citrate may be more effective than potassium citrate alone.[20]
Dietary salt intake has long been known to contribute increased calcium loss
in the urine in both normal subjects and in those with hypercalciuria.[21] [22]
[23] [24]
A study of normal subjects found that increasing dietary salt from 50 to 250
mmol/day increased urinary calcium from 2.73 to 3.93 mmol/day or 44%. This
increase in salt intake also significantly reduced urinary citrate from 3.14
to 2.52 mmol/day or about 20%. As a result of this increase in calcium and decrease
in citrate the tendency for calcium phosphate, uric acid and calcium oxalate
to crytallize all increased significantly.[25]
Kidney stones can now be added to the long and growing list of diseases linked
to the amount of salt in the average American’s diet. Excessive salt intake
increases the risk of kidney stones, osteoporosis, hypertension, stroke, kidney
failure and heart disease and also may promote stomach and kidney cancer.[26]
Because the dangers of excessive salt intake are many and the risk of reducing
dietary salt intake are extremely uncommon it seems wise to encourage all patients
with a history of kidney stones to reduce their salt intake to no more than
1000 to 1500 mg Sodium daily. The one caveat for patients greatly reducing their
salt intake is to encourage them to keep their fluid high because with a low-salt
diet thirst will be reduced.
A recent 5 year randomized controlled study compared the effects of two diets
in 120 men with recurrent calcium oxalate stones. On one experimental diet animal
protein was reduced (to a target of 52 gm/day) and dietary salt intake was cut
by about 50% (the target was actually only 1150 mg sodium/day). The risk of
new kidney stone formation over 5 years was reduced by 51% in the low-salt and
meat group compared to the second group in which calcium intake was reduced
to only 10 mmol per day (400 mg/day).[27]
Neither salt or animal protein intake was reduced in the low-calcium group.
The calcium intake of the low-salt and animal protein diet was not limited and
the amount consumed was about 30 mmol/day (1200 mg calcium/day). The authors
of this study conclude, “In men with recurrent calcium oxalate stones and hypercalciuria,
restricted intake of animal protein and salt, combined with a normal calcium
intake, provides greater protection than the traditional low-calcium diet.”
This study clearly demonstrates that restricting the intake of meat and salt
is far more effective at preventing kidney stone formation than a diet that
merely limits calcium intake.
It is important for physicians to rule out secondary causes of kidney stone
formation. When infection, hyperparathyroidism and renal tubular acidosis are
promoting kidney stone formation it is important that this primary disease process
be the focus of medical treatment.[28]
Once secondary causes have been ruled out the patient should be referred for
dietary counseling.
In addition to dietary counseling physicians may utilize various pharmacological
agents such as thiazide diuretics, phosphates, allopurinol and potassium citrate
to treat patients with recurrent calcium oxalate kidney stones. However, none
of these agents have been proven as effective as a high fiber diet low in salt,
animal protein and oxalate rich foods.[29]
All medications can have adverse side effects. Because a diet lower in animal
protein, salt and higher in fiber has other health benefits it seems reasonable
for physicians to emphasize dietary therapy for the treatment and prevention
of kidney stones. Medical intervention if dietary therapy fails can usually
successfully treat stones with lithotripsy. The benefits of reduced stone formation
from prescription drug therapy is unlikely to prove greater than the long-term
adverse effects associated with the use of the pharmaceutical agents. However,
physicians may want to consider the use of supplemental potassium-magnesium
citrate as an adjunct to dietary therapy particularly in patients who do not
comply with the low salt and meat diet.
Kidney stones are known to result from a variety of metabolic and nutritional
factors in genetically susceptible individuals. These include hypercalciuria,
hypocitraturia, hyperoxaluria and a low urine volume. To a large extent the
typical Western diet that is low in fiber, potassium, citrate, and magnesium
and high in animal protein, purines, salt and often supplemented with high doses
of calcium and vitamin C will promote kidney stone formation in genetically
susceptible individuals. By contrast, a more vegetarian diet that is rich in
potassium, magnesium, citrate, fiber and restricted in oxalic acid rich foods
and salt coupled with an increased fluid intake should help prevent or at least
greatly reduce the recurrences of kidney stones in most patients.
[2] Ramello A, Vitale C, Marangella M.
Epidemiology of nephrolithiasis. J Nephrol 2000;13(suppl3):S45-50
[3] Robertson WG, Peacock M. The cause
of idiopathic calcium stone disease: Hypercalciuria or hyperoxalauria? Nephron.
1980;26:105-10
[4] Broadus AE, Insogna KL, Lang R, et
al. Evidence for disordered control of 1,25-dihydroxyvitamin D production
in absorptive hypercalciuria. N Engl J Med 1984;311:73-80
[5] Epstein FH. Calcium and the kidney.
Am J Med 1968;45:700-14
[6] Marshall RW, Cochrane M, Hodgkinson
A. Relationship between calcium and oxalic acid intake in the diet and their
excretion in the urine of normal and renal-stone-forming subjects. Clin Sci
1972;43:91-9
[7] Curhan GC, Willett WC, Rimm EB, Stampher
MJ. A prospective study of dietary calcium and other nutrients and the risk
of symptomatic kidney stones. N Engl J Med 1993;328:833-8
[8] Curhan GC, Willett WC, Spezer FE, et
al. Comparison of dietary calcium with supplemental calcium and other nutrients
as factors affecting the risk for kidney stones in women. Ann Intern Med 1997;126:497-504
[9] Ettinger B, Pak CY, Citron JT, VanGessel
A. Potassium magnesium citrate is an effective prophylaxis against recurrent
calcium oxalate nephrolithiasis. J Urol 1997;158:2069-73
[10] Massey LK, Roman-Smith H, Sutton
RA. Effect of dietary oxalate and calcium on urinary oxalate and the risk
of formation of calcium oxalate kidney stones. J Am Dietet Assoc 1993;93:901-6
[11] Lindberg JS, Sprague S. Nephrolithiasis:
Causes and treatment. J Critical Illness 2001;16:446-59
[12] Sutton RA, Walker VR. Enteric and
mild hyperoxaluria. Miner Electrolyte Metab 1994;20:352-60
[13] Allen LH, Oddoye EA, Margen S. Protein
induced hypercalciuria: a longer-term study. Am J Clin Nutr 1979;32:741-9,
Zemel MB, Schutte SA, Hegsted Linkswiler HM. Role of sulfur-containing amino
acids in protein induced hypercalciuria in men. J Nutr 1981;111:545-52
[14] Robertson WG, Peacock M, Heyburn
PJ, et al. Should recurrent calcium oxalate stone formers become vegetarians?
Br J Urology 1979;51:427-31
[15] Giannini S, Nobile M, Satori L, et
al. Acute effects of moderate dietary protein restriction in patients with
idiopathic hypercalciuria and nephrolithasis. Am J Clin Nutr 1999;69:267-71
[16] Pak CY, Sakhaee K, Fuller C. Successful
management of uric acid nephrolithiasis with potassium citrate. Kidney Int
1986;30:422-8
[17] Hiatt RA, Ettinger B, Caan B, et
al. Randomized controlled trial of a low animal protein, high-fiber diet in
the prevention of recurrent calcium oxalate kidney stones. Am J Epidemiol
1996;144:25-33
[18] Robertson WG, Peacock M, Heyburn
FA, et al. Should recurrent calcium oxalate stone formers become vegetarians?
Br J Urology 1979;51:427-31
[19] Pak CY. Kidney Stones. Lancet 1998;351:1797-801
[20] Ettinger B, Pak CY, Citron JT, Van
Gessel A. Potassium magnesium citrate is an effective prophylaxis against
recurrent calcium oxalate nephrolithiasis. J Urol 1997;158:2069-73
[21] Kleeman CR, Bohannan J, Bernstein
D, et al. Effect of variations in sodium intake on calcium excretion in normal
humans. Proc Soc Exp Biol Med 1964;115:29-32
[22] Phillips MJ, Cooke JN. Relation between
urinary calcium and sodium in patients with idiopathic hypercalciuria. Lancet
1967;1:1374-7
[23] Muldowney FP, Freaney R, Moloney
MF. Importance of dietary sodium in the hypercalciuria syndrome. Kidney Int
1982;22:292-6
[24] Silver J, Rubinger D, Friedlaender
MM, Popovetzer MM. Sodium-dependent idiopathic hypercalciuria in renal-stone
formers. Lancet 19832:484-6
[25] Sakhaee K, Harvey JA, Padalino PK,
et al. The potential role of salt abuse on the risk of kidney stone formation.
J Urology 1993;150:310-2
[27] Borghi L, Schianchi T, Meschi T,
et al. Comparison of two diets for the prevention of recurrent stones in idiopathic
hypercalciuria. N Engl J Med 2002;346:77-84
[28] Curhan GC, Curhan SG. Dietary factors
and kidney stone formation. Comp Therapy 1994;20:485-9
[29] Goldfarb S. The role of diet in the
pathogenesis and therapy of nephrolithiasis. Endo Metab Clin N Amer 1990;19:805-20