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Diet and Kidney Stones � 2 CPE Hours

Good through December 2016

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

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.

What Diet Is Appropriate For Patients With Nephroliathiasis?

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                                


Triple Phosphate                                        


Calcium phosphate                                       




Uric Acid                                                




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.

Should Dietary Calcium Be Restricted?

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.

Should Dietary Oxalate Be Reduced?

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



Oxalate (mg)

Calcium (mg)*

Beet greens, cooked

1/2 cup




Rhubarb, stewed, no sugar

1/2 cup




Spinach, cooked

1/2 cup




Beets, cooked

1/2 cup




Swiss Chard, cooked

1/2 cup




Spinach, frozen

1/2 cup




Cocoa, dry

1/3 cup




Okra, cooked

1/2 cup




Sweet potatoes, cooked

1/2 cup





1/3 cup





1 cup




Pecans, halves

1/3 cup




Wheat germ

1/4 cup




*Note: Foods with a high oxalic acid to calcium ratio increase oxalic acid in the urine.

Should Dietary Protein Be Restricted?

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.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]

Is It Necessary To Limit Salt Intake?

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.

It Is Better to Reduce Salt and Animal Protein than Calcium

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.

Medical Treatment of Kidney Stones

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.


[1] Kidney and urologic diseases statistics for the United States. Bethesda, Md.: National Institute of Diabetes & Kidney Diseases, 2001. (Assessed Dec. 18,2001,at

[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


[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

[26] Kenney JJ. Salt: Has it been given a fair shake? Or is it a serial killer?

[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

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