by Jack Norris, RD • Last updated December 2013
- Digestive Disorders
- Vitamin C
- Vitamin B6
- Fungal Infections
- Green Smoothies
- Is the Average Vegan at Risk of Too Much Oxalate?
- The DASH Diet
- Oxalate and a Vegetarian Diet
- Decreasing Absorption of Oxalate from Foods
- Decreasing Calcium-Oxalate Formation in the Kidney for Stone Prevention
- Potassium Citrate
- Calcium Citrate
- Beverages and Stone Occurrence
- Beverages and Stone Markers
- Iron Absorption
- Oxalate Content of Foods
- Other Resources
Oxalate is a molecule many in the vegan community are familiar with for preventing the absorption of calcium. This article does not address that subject—info can be found in the section Calcium Absorption from Plant Foods.
Oxalate is also known for the part it plays in calcium-oxalate kidney stones, which is the most common form of kidney stone.
In many cases, getting a kidney stone is a one-time thing and does not occur again. Increasing fluid intake can cut the incidence of getting another stone in half. Cutting down on the amount of oxalate in the diet is another strategy for reducing stone recurrence. Some calcium-oxalate stone formers are prescribed potassium-citrate tablets which are also effective at reducing stones.
Oxalate is generally not found in animal products while many plant foods are moderate or high, and some are extremely high (such as spinach, beets, beet greens, sweet potatoes, peanuts, rhubarb, and swiss chard). Despite this, a study from the Harvard School of Public Health found that people following a plant-based eating pattern had a lower occurrence of kidney stones (59).
There is no research on kidney stone frequency in vegans, though anecdotally I know of some who have gotten stones. Of course, meat-eaters also get kidney stones—but is the average vegan at a higher or lower risk? Vegan diets are higher in some elements that increase the risk of stones, lower in some, and higher in some things that prevent stones, so it is hard to say.
The story regarding oxalate does not end with kidney stones. There is currently an entire community built around the idea that absorbing too much oxalate, known as enteric hyperoxaluria, either causes or exacerbates many diseases such as fibromyalgia, interstitial cystitis, vulvodynia, depression, arthritis, autism, and a variety of digestive disorders (which, in turn, exacerbate hyperoxaluria by allowing even more oxalate to be absorbed).
According to LowOxalate.info, leaky gut syndrome, in which molecules are absorbed from the digestive tract at a higher than normal rate, can cause hyperoxaluria. They also say that you cannot rely on getting a kidney stone as a warning sign before oxalate accumulates in other tissues.
There is not much research (on humans) regarding hyperoxaluria and diseases other than kidney stones and vulvodynia, so it is hard to say much about them with any certainty. However, many people have reported improved health on a low-oxalate diet and given the high amount of oxalate in some plant foods, it might be a good idea for vegans to be aware of this issue and not eat unusually high amounts of these foods.
Here are some other tips for minimizing problems from oxalate:
- Boil high-oxalate leafy greens and discard the water.
- Meet the RDA for calcium. Eat high-calcium foods or take calcium with meals; calcium citrate if you have a history of calcium-oxalate stones.
- Drink plenty of fluid.
- Do not include large amounts of high-oxalate vegetables in your green smoothies.
- Do not take large amounts of vitamin C.
If you have a history of calcium-oxalate kidney stones or suspect you have hyperoxaluria, there are a few more things you can do such as limit oxalate as much as possible, add citrate to your diet (through orange or lemon juice, or calcium citrate), minimize added fructose and sodium, or try a probiotic supplement as described below.
Please see the Contents above for quick links to more details about all of these topics as well as tables of the oxalate content of foods and other helpful resources.
Oxalate is a small molecule found in large amounts in many plants foods but not found in animal foods. Our bodies make oxalate as an end product of metabolism (primarily the metabolism of the protein amino acids glycine and serine, but also of vitamin C and possibly fructose). However, our bodies do not use oxalate in any way, nor degrade it, and it must be excreted through the urine or feces. Even if oxalate intake is zero, oxalate will be excreted in the urine as a result of normal metabolism.
Oxalate is made of two carbons and four oxygen with a charge of -2, making it attracted to other molecules with a charge of +2; especially calcium and to a lesser extent magnesium. When oxalate combines with calcium in urine, it becomes insoluble (i.e., a solid). If enough calcium-oxalate crystals form in the bladder, kidney stones can develop.
In the USA’s National Health And Nutrition Examination Survey (NHANES) 2007–2010, the rate of having had a kidney stone was 10.6% for men and 7.1% for women (60). Approximately 25% of untreated patients experience a new episode within 5 years (60).
Calcium-oxalate is the most common form of kidney stones, accounting for about 75%. It is essential to determine the type of stone (calcium-oxalate, calcium-phosphate, uric acid, cystine, or struvite) as treatment methods can conflict.
An increased level of oxalate in the urine is a risk for calcium-oxalate kidney stones. For adults, this is considered to be above 45 mg per day.
When someone with a kidney stone is tested for various metabolic defects that can cause kidney stones (such as kidney problems that cause acidosis) and none are found, their kidney stone is labeled “idiopathic.” A large proportion of kidney stones are considered idiopathic and they are typically calcium-oxalate.
A 2006 study from the University of Bonn compared oxalate absorption between 120 kidney stone formers and 120 non-formers on low-oxalate diets with equal amounts of oxalate (63 mg/day) and calcium (800 mg/day) (56). None of the participants had a history of digestive disorders (which can increase oxalate absorption). They found a small, but statistically significant difference in oxalate absorption between stone formers (10.2%) and controls (8.0%). There were no gender or age differences. Of the oxalate absorbed within 24 hours, 80-85% of it was absorbed within the first 6 hours after ingestion. Absorption values greater than 20% only occurred in the stone formers. When extrapolated to higher oxalate diets, the researchers believed that “Oxalate hyperabsorption may be the main reason for stone formation in more than half of the idiopathic calcium oxalate stone formers.”
Another study found oxalate to be absorbed at a very low rate of .75 to 1.9% (35).
Based on 5 individuals, researchers from Wake Forest University estimated the daily intake of oxalate to be an average of 152 ± 83 mg, ranging from 44 – 352 mg/day. Samples of the food were analyzed for oxalate content; in other words, the amounts were not simply based on food tables (9).
Patients with idiopathic kidney stones tend to have high rates of osteopenia and osteoporosis. One study showed that 50% had osteopenia and 16% had osteoporosis (57). In another study, 56% of male and 50% of female stone formers had osteopenia while 10% of the men and 24% of the women had osteoporosis (58).
Hyperoxaluria is a condition in which the amount of oxalate in the urine becomes very high, so high that it can cause severe kidney damage. Oxalosis refers to oxalate deposits in the kidney.
There are two types of hyperoxaluria, primary and enteric.
Primary hyperoxaluria is a genetic disease in which the liver produces too much oxalate. It occurs in 1 out of 100,000 to 1 million people (1).
Enteric hyperoxaluria is when too much oxalate is absorbed from the digestive tract. This typically happens in cases of intestinal diseases and more rarely in cases of very high-oxalate diets.
In cases of hyperoxaluria, it is possible that the build-up of oxalate in the body can become so great that it doesn’t just damage the kidneys, but can be deposited in other parts of the body. This has led to much speculation that people suffering from diseases other than kidney stones are actually suffering from an accumulation of oxalate in other tissues.
If you suspect that you are suffering from hyperoxaluria, you should talk to a health professional. The Mayo Clinic has some helpful information in their article Hyperoxaluria and oxalosis as does the Oxalosis and Hyperoxaluria Foundation (OHF).
Because kidney stones are rare in childhood, the OHF recommends that all children and adolescents who have symptoms of kidney stones be screened for hyperoxaluria (more info).”
Current practice (as of October 2013) is that if a low-oxalate diet is adhered to but does not succeed in lowering urinary oxalate levels, the low-oxalate diet can be abandoned because dietary oxalate is not the cause. Very high-oxalate foods should still be avoided.
LowOxalate.info is a popular website that provides support for people suffering from hyperoxaluria. They suggest that hyperoxaluria may play a significant role in autism, COPD/asthma, and thyroid disease. They say that, “So far, our list of conditions that improve [upon reducing oxalate intake] includes fibromyalgia, interstitial cystitis, vulvodynia, depression, arthritis, and gut problems of all sorts, as well as autism and many other developmental disorders.”
Of problems that do not involve the kidney that could be caused by hyperoxaluria, vulvodynia appears to be the most studied. Vulvodynia is when the vulva becomes very painful upon touch or pressure. Hyperoxaluria could lead to oxalate crystals forming in these sensitive tissues causing the pain.
There is a 1991 case report in the Journal of Reproductive Medicine, in which a woman who had suffered from vulvodynia for four years was given calcium citrate to reduce the oxalate levels in her body. After a year, she was pain-free. Upon discontinuing the calcium citrate, her symptoms returned only to disappear again after reintroduction of the calcium citrate (2).
A 1997 study from Good Samaritan Hospital in Cincinnati showed some mixed results on oxalate and vulvodynia (3). They were not able to predict vulvar pain by measuring oxalate excretion. However, a small number of women (5 out of 59) appeared to have cured their vulvodynia using 400 mg of calcium citrate 3 times a day, while 9 others improved.
A 1999 case-control study from the University of Michigan found that women with vulvar vestibulitis syndrome (VVS), a form of vulvodynia, consumed more high and medium rather than low oxalate foods, but there was no significant difference in average oxalate intake based on a questionnaire regarding the previous 4-weeks (75). Bacterial vaginosis, yeast infections, and human papillomavirus were strongly associated with VVS.
A 2008 study from the University of Minnesota found no association between oxalate intake in vulvodynia cases vs. controls when oxalate intake was divided into low, medium, and high (intake amounts were not reported; 4).
As for the other diseases listed by LowOxalate.info, there isn’t much research:
- A 2012 study from Poland found that blood and urinary oxalate were significantly higher in kids with autism. Trials are being conducted to see if a low-oxalate diet will improve symptoms (7).
- Oxalate deposits are common in the human thyroid (8), but there was no more research than that.
- Digestive disorders – Hyperoxaluria is common in Crohn’s disease (see below), but is not considered to be a cause. I could not find any research on irritable bowel syndrome and very little on ulcerative colitis.
- I found no research on asthma, arthritis, fibromyalgia, interstitial cystitis, or depression.
Fat malabsorption results in unabsorbed fat forming insoluble soaps with calcium. This prevents calcium from being available to combine with oxalate in the gut, resulting in a higher oxalate absorption (52).
Short bowel syndrome, in which part of the bowel is surgically removed, is a common reason for fat malabsorption. Short bowel syndrome is common in people with Crohn’s disease and in bariatric surgery.
Patients with Crohn’s are more likely to have hyperoxaluria, and this hyperoxaluria is more common in Crohn’s patients who have had a bowel resection (part of their digestive tract removed). Such patients are at a higher risk of calcium-oxalate kidney stones and in some cases oxalosis results and can cause kidney failure.
The hyperoxaluria in Crohn’s patients is thought to be caused by enteric hyperoxaluria (an increase of oxalate absorption), but could also be exacerbated by other factors, such as fat, vitamin B6, calcium, magnesium, and citrate malabsorption.
A 2012 study from Germany found that 28% of Crohn’s patients had calcium-oxalate kidney stones. These patients had an average oxalate absorption rate of 23%, compared to 8% in the patients without kidney stones (42).
The authors of the study note a case in which a young woman with Crohn’s suffered from end-state renal failure at age 34. Her first kidney transplant failed due to hyperoxaluria. Her second transplant succeeded due to extra pre-transplant hemodialysis and vitamin B6, and post-transplant fluids, citrate, and O. formigenes administration.
The authors conclude that “[T]he high prevalence of [kidney stones]/oxalosis in patients with Crohn’s disease is based on secondary, enteric hyperoxaluria. Conservative treatment options are still scarce and only a high fluid intake plus careful dietary advice (low-oxalate and slightly enriched calcium diet) are the current therapeutic measures.”
People with short bowel syndrome can suffer from a lack of bile acid absorption. A 2003 study from Baylor University provided patients with bile acid replacement therapy for 3 days resulting in significantly less urinary oxalate excretion, from 87 to 64 mg per day (52). In the one patient followed, 3 months of treatment (of not only bile acid replacement), resulted in a further reduction to 27 mg of oxalate excreted per day.
Natural bile acids are not vegan, but there is a synthetic version, cholylsarcosine, which also reduced urinary oxalate excretion from 87 to 73 mg per day in the 3-day Baylor University study. I was not able to determine if cholylsarcosine is vegan.
Oxalate can be a byproduct of vitamin C metabolism. The RDA for vitamin C is 90 mg for adult men and 75 mg for adult women.
A 2004 report from the Health Professionals Follow-up Study found an increased risk of kidney stones among men getting more than 1,000 mg of vitamin C per day compared to those getting 90 mg/day or less (1.41, 1.11-1.80) (12). A 1999 report from the Nurses Health Study did not find an association between high vitamin C intakes (above 1500 mg) and risk of kidney stones (43).
Even though large amounts of vitamin C can be broken down into oxalate, and people at risk for kidney stones should not take vitamin C tablets, this does not necessarily mean they should not drink orange juice, which contains other molecules that can be beneficial for kidney stones, especially potassium and citrate.
The Health Professionals Follow-up Study found an association between total fructose intake and risk of kidney stones in men (1.28. 1.06–1.55) for highest versus lowest fructose intake of 13.8% vs. 5.6% of calories. The Nurses Health Study I (of older women) and II (of younger women) found similar results. Similar results were found for absolute amounts of fructose, and not just as a percentage of calories (55).
In a 1995 study, researchers from France found that giving fructose intravenously caused an increase in urinary oxalate, while glucose did not (76). Interestingly, an oral load of fructose had the opposite effect, reducing urinary oxalate. Fructose also increased uric acid levels in the blood, but not in urine, which could be relevant to uric acid kidney stones.
Vitamin B6 deficiency could possibly play a role in hyperoxaluria. The authors of a paper on Crohn’s say, “It is known that in states of low serum vitamin B6, the cofactor of the glyoxylate transaminating liver enzyme alanine:glyoxylate-aminotransferase (AGT), may lead to accumulation of peroxisomal glyoxylate, which is later oxidized to oxalate (42).”
In a 1996 report, the Health Professionals Follow-up Study did not find an association between vitamin B6 intake and kidney stones, comparing men consuming 40 mg per day to those consuming less than 3 mg (who had an average intake of 2 mg) (44). A 2004 report from that study also found no association after 14 years of follow-up (12). The RDA for vitamin B6 is only 1.3 mg for adults 18 to 50 years old and 1.7 for men over 50, so very few, if any, of these men were likely suffering from vitamin B6 deficiency.
A 1999 report from the Nurse’s Health Study also did not find an association between low vitamin B6 intake and kidney stones, but the lowest intake level met the RDA so, again, there were probably few people in the study with B6 deficiency (43).
An article by Dr. William Shaw of The Great Plains Laboratory, Oxalates: Test Implications for Yeast & Heavy Metals, suggests that fungal infections could produce a high oxalate burden on the body. I could not find much research on humans regarding this, but it’s something people with fungal infections might want to consider or talk to their health professional about.
Someone eating high-oxalate greens for green smoothies could end up with an unusually high oxalate intake which could possibly lead to a kidney stone.
In 2012, the Mayo Clinic reported on an 81-year old man with kidney failure apparently brought on by juicing high-oxalate vegetables in an attempt to lose weight. His dietary oxalate intake while juicing averaged 1,260 mg and ranged from 35 – 5,000 mg (10). He also had a high daily intake of vitamin C of 150 – 900 mg from his diet plus 2,000 mg from a supplement. His calcium intake was low, averaging 370 mg/day. All of these factors likely contributed to his oxalosis, and his age could have been a factor since kidney function decreases with age.
When you pull all this information together, the man created a perfect storm for kidney problems from a huge oxalate load, no boiling out of soluble oxalate (more info below), large amounts of vitamin C, and a low calcium intake limiting the creation of insoluble oxalate in his digestive tract (more info below).
Apparently, there are numerous anecdotal reports of people who take up green smoothies and subsequently develop kidney stones.
Is the Average Vegan at Risk for Kidney Stones?
A 2014 study from EPIC-Oxford measured the risk of being hospitalized for a kidney stone over the course of five years for people in various diet groups (77). Vegetarians (including vegans) had a 31% lower risk (.69, .48–0.98) as compared to high meat-eaters.
While people who have had calcium-oxalate kidney stones need to watch their oxalate intake, the evidence that a diet moderately high in oxalate puts the average person at risk for kidney stones is not strong.
The Health Professionals Follow-up Study (HPFS) and the Nurses’ Health Studies I and II are two of the of largest and best designed prospective studies on nutrition and health. In 2007, they reported an increased risk of kidney stones for men between the highest one-fifth of oxalate intake (median of 328 mg/day) compared to the lowest one-fifth (median of 106 mg/day) of 1.22 (1.03- 1.45). For older women, the risk for the highest one-fifth (median of 287 mg/day) compared to the lowest one-fifth (87 mg/day) was 1.21 (1.01-1.44). There was no association for younger women. Being below the median calcium intake of 755 mg/day strengthened the association a bit for men 1.46 (1.11-1.93) (30).
Despite the statistically significant findings, the author’s conclude, “Our data do not support the contention that dietary oxalate is a major risk factor for incident kidney stones. The risk that was associated with oxalate intake was modest even in individuals who consumed diets that were relatively low in calcium.”
To put this in some perspective, my calculations show that being in the highest one-fifth of oxalate intake would raise the risk of getting a kidney stone from age 20 to 70 from 17% to 21% (31) for men. These calculations are somewhat crude, assuming the risk is over 50 adult years and without adjusting for the fact that different fifths of this population had different risk rates, but they’re probably in the ballpark.
The DASH Diet
Dietary Approaches to Stop Hypertension (DASH) is a diet high in fruits and vegetables, moderate in low-fat dairy products, low in animal protein, and usually low in sodium. This diet has been used to successfully reduce blood pressure in people with hypertension.
The Harvard School of Public Health thought that a DASH eating pattern might help prevent kidney stones so they tested it in their three big cohorts (Health Professionals Follow-up Study and the Nurses Health Studies I and II) (59). They found that those eating a DASH-like diet pattern at baseline had about half the risk of kidney stones. Comparing the highest one-fifth to the lowest, in regards to DASH score, the rates were .55 (0.46-0.65) for men, 0.58 (0.49-0.68) for older women, and 0.60 (0.52-0.70) for younger women. The lower risk was independent of age, body size, hypertension, diabetes, thiazide use, and intakes of total calories, fluid, caffeine, and alcohol. The type of kidney stone was not determined in this study, but it can be assumed that most were calcium-oxalate.
Animal protein ended up not varying much across the groups, so that wasn’t the protective factor. Calcium went up with higher DASH scores, but even at low calcium intakes, higher DASH scores had lower rates of kidney stones.
The researchers state:
The consistent association between consumption of a DASH-style diet and lower kidney stone risk in all three cohorts is remarkable considering the substantial differences we previously observed in individual dietary factors and risk between men (HPFS), older women (NHS I), and younger women (NHS II).
Although we think it reasonable for calcium oxalate stone formers with high levels of urinary oxalate to avoid intake of some individual foods very high in oxalate (such as spinach and almonds), our data do not support the common practice of dietary oxalate restriction in calcium stone formers, particularly if such advice results in lower intake of fruits, vegetables, and whole grains.
Oxalate and a Vegetarian Diet
There are no studies measuring oxalate levels or kidney stone risks in vegans. However, there are some trials investigating the effects of a vegetarian diet on kidney stone risk.
In 1979, researchers from the General Infirmary in Leeds, UK, asked, “Should recurrent calcium oxalate stone formers become vegetarians?” (16) These researchers wanted to investigate the connection between animal protein and kidney stones.
Twenty-four-hour urines were collected from 22 lacto-ovo vegetarians (10 male and 12 female) and analyzed for 6 risk factors. The vegetarians had a slightly lower risk of forming stones than meat-eating women, a bit more than meat-eating men, and a lot lower than previous stone formers. Urinary oxalate excretion for the vegetarians was about 27.8 mg/day compared to about 44.4 mg/day for recurrent stone formers.
In 2002, researchers from the University of Bonn in Germany studied the effects of four different diets on the urine of 10 men with no history of kidney stones (17). All the men ate each diet for a period of five days each. The diets included:
- The men’s standard diet (SD)
- A typical Western diet of high energy, alcohol and purine content, excess protein, and low fluid (WD)
- Normal diet (ND)—not really defined but supposedly healthier than the WD
- A lacto-ovo vegetarian diet (VD)
All the test diets contained about 800 mg of calcium.
The risk of calcium oxalate crystallization was highest on the SD and WD diets with no difference between the ND and VD. The VD had lower urinary calcium, which lowers stone risk, but higher urinary oxalate. The authors suggested that on a vegetarian diet, calcium intake should be even higher than 800 mg to help bind more oxalate in the digestive tract.
A 2008 study was conducted by the Bonn researchers on 8 healthy volunteers (3 men, 5 women) with no history of kidney stones (18). Each person took turns eating a low-oxalate omnivore diet, a low-oxalate (70 mg) vegetarian diet, and a high-oxalate (300 mg) vegetarian diet.
|Table 1. Oxalate Metabolism in 3 Diets18|
|Supersaturation of Ca-Ox|
|Ca-Ox – calcium-oxalate.|
The researchers were surprised that the higher oxalate vegetarian diet resulted in less oxalate absorbed and excreted through the urine than the low-oxalate vegetarian diet (see Table 1). They attributed it to the fact that the highest oxalate meal (251 mg from spinach) in the high-oxalate diet contained a cream sauce providing 212 mg of calcium, which could have negated the higher oxalate load. This seems reasonable, but there is still a question as to why more oxalate was excreted in the urine and the supersaturation was higher on the low-oxalate diet. In any case, the researchers believed that a vegetarian diet must contain enough calcium at meals to prevent oxalate absorption if they are going to be prescribed for people with kidney disease, though I don’t see how that could be concluded from this study.
The authors were also concerned about the binding of calcium by phytate in high-oxalate vegetarian meals as this could reduce the available calcium for binding with oxalate. Other research has shown that unless phytate is present in unusually high amounts, such as in wheat bran, it probably does not bind much calcium (19).
In summary, the research seems to indicate that if oxalate is not higher than 300 mg and calcium intake is adequate, the average plant-based eater should not be at a higher risk for kidney stones than the average person.
Decreasing Absorption of Oxalate from Foods
Soluble vs. Insoluble
Oxalate in food is either soluble or insoluble. Insoluble oxalate is bound to another molecule that makes it much harder to absorb; normally calcium but also sometimes magnesium. Calcium supplements are often recommended for oxalate kidney stone patients to bind with oxalate and be excreted (more info below).
Soluble oxalate is not attached to another molecule and is more easily absorbed.The intake of soluble oxalate might be much more important than total oxalate.
For example, in a 2008 study from the University of Wyoming, subjects without a history of kidney stones were given just over 1 teaspoon of cinnamon (3.5 g) or 3.2 g of turmeric, each providing 63 mg of oxalate, broken into 3 doses per day for 4 weeks with meals (41). In turmeric, 91% of the oxalate was soluble, while only 6% of the oxalate in cinnamon was soluble. Turmeric caused significantly higher urinary oxalate for the 6-hour and 22-hour tests, while cinnamon did not show a significant increase.
It is, however, at least theoretically possible that if someone has a “leaky gut”, where there are gaps in the junctions between cells in their intestinal walls, they could absorb large amounts of both soluble and insoluble oxalate.
A number of studies have found that boiling plants allows much of the soluble oxalate to escape into the boiling water which can then be discarded (13). University of Wyoming researchers measured the oxalate levels in a variety of vegetable using different cooking methods (14). Boiling reduced total oxalate levels by a decent amount, steaming to a lesser extent (Table 2). The study showed that the majority of the oxalate lost was soluble.
The authors write, “There was a significant loss of soluble oxalate in almost all test vegetables by boiling, ranging from 30 to 87%. It also appears that oxalate is much easier lost from leaves than from stalks and roots.”
One caveat to this study is that many of these vegetables were cooked for a much longer time than might be typical. For example, spinach was boiled for 12 minutes, which seems to be at least twice as long as a normal boiling time.
|Table 2. Oxalate Content (mg per 100 g wet weight)14|
|red swiss chard||12||1,167||1,052||10%||428||63%|
|green swiss chard||12||964||556||42%||335||65%|
Adding calcium to meals could decrease the available soluble oxalate resulting in less oxalate absorbed.
A 2003 study from Lincoln University in New Zealand measured the oxalate absorption from spinach with calcium added to the diet (35). The spinach contained 957 mg of oxalate, of which 737 mg was soluble. The spinach was grilled to prevent loss of soluble oxalate into cooking water. The spinach contained 90 mg of calcium, of which 69 mg was bound to oxalate. The mean bioavailability of soluble oxalate in the grilled spinach was 0.75 ± 0.48% over a 6-hour period after intake and was 1.93 ± 0.85% measured over a 24-hour period. Adding 117 mg of calcium from sour cream reduced the 6-hour oxalate absorption to .52%. Adding 480 mg of calcium from sour cream and milk reduced the absorption to .14%. Adding 80 mg of calcium from cottage cheese did not reduce absorption.
In a 1993 report, the Health Professionals Follow-Up Study (men) found an increased risk of kidney stone in the lowest one-fifth of calcium intake of < 605 mg/day compared to all other fifths, the highest category having a median intake of 1,326 mg per day (36). Animal protein intake was also associated with a higher risk of kidney stones, whereas potassium and fluid intake was associated with a lower risk. Sodium, magnesium, phosphorus, sucrose, and fiber were not associated with risk.
A 1997 report from the Nurse’s Health Study I, conducted on older women, found that the highest one-fifth intake of dietary calcium (not including supplements, median intake of 1,303 mg/day) was associated with a significantly lower risk of kidney stones than the lowest intake (median 391 mg/day) (37). Supplemental calcium didn’t fare as well; it increased risk (1.20, 1.02-1.41). Sucrose and sodium intake were associated with an increased risk, while potassium and fluid were associated with a decreased risk. Intake of animal protein, phosphorus, and magnesium were not significantly associated with risk.
A 2004 report from the Nurse’s Health Study 2, conducted on younger women, found that those in the lowest one-fifth of dietary calcium (median 540 mg/day) had a higher risk of kidney stones compared to the highest one-fifth (median 1,300 mg/day) (38). There was a statistically significant trend towards lower kidney stones among the intermediate categories. Supplemental calcium was not associated with a reduced risk. Animal protein was marginally associated with decreased risk. Phytate and total fluid intakes were significantly related to reduced risk. Sucrose intake was associated with an increased risk, while the intakes of sodium, potassium, magnesium, and phosphorus were not independently associated with risk.
The researchers said that most of the women were not taking their calcium supplements with meals and this could explain why the supplements were not reducing their risk (38).
Degradation by Intestinal Bacteria
There are a number of common intestinal bacteria that degrade oxalate, reducing the oxalate load of the body. Oxalobacter formigenes is the most studied of these bacteria.
A 2012 paper from Wake Forest University reports that the rates of people who have O. formigenes in their digestive tracts range from from 38% in the USA to 77% in Korea (20). They say, “Colonization rates are much lower in diseases where the bowel is affected, such as inflammatory bowel disease and cystic fibrosis. Such patients are known to have increased oxalate excretion and supersaturation of calcium oxalate, and are also at risk for developing kidney stones.”
One reason some people might have high levels of oxalate is that antibiotic therapy has killed the O. formigenes in their digestive tract. There are a number of strains of O. formigenes and some are sensitive to some antibiotics while others are not. The Wake Forest University team determined that all four O. formigenes strains they tested were resistant to amoxicillin, amoxicillin/clavulanate, ceftriaxone, cephalexin, and vancomycin. All four strains were sensitive to azithromycin, ciprofloxacin, clarithromycin, clindamycin, doxycycline, gentamicin, levofloxacin, metronidazole, and tetracycline. One strain was resistant to nitrofurantoin while the others were sensitive (20).
Being sensitive to an antibiotic in vitro does not necessarily mean that someone’s O. formigenes will be wiped out by treatment with that antibiotic. A 2011 study by New York Harbor Veterans Affairs Medical Center and Bellevue Hospital found that 7 out of 16 patients receiving amoxicillin/clarithromycin were still colonized with O. formigenes after 6 months, whereas 2 treated with metronidazole/tetracycline/bismuth and 1 treated with metronidazole/clarithromycin were not (21).
A 2008 case-control study conducted with patients from hospitals from Boston and North Carolina found that only 17% of people with recurrent kidney stones had O. formigenes in their stool, compared to 38% of the control group (22). The presence of O. formigenes among cases was highest in the one-third with the highest oxalate intake. Based on a number of other findings in the study, the researchers suggest that O. formigenes may prevent a post-meal spike in urinary oxalate while not doing much to change the total urinary oxalate over a 24-hour period. There is some thought that urinary oxalate spikes are more important than overall oxalate loads in contributing to stone formation.
A 2011 study from Wake Forest found that 24-hour urinary oxalate excretion was 20% lower on a low calcium (400 mg), moderate oxalate (250 mg) diet in people colonized with O. formigenes (23). This indicates that when calcium intake is low, O. formigenes might have more of an impact. Higher calcium intakes reduced the amount of O. formigenes, indicating that calcium may bind with oxalate and prevent the feeding of O. formigenes.
In a 2013 study, Bonn researchers found that among kidney stone formers, O. formigenes did not decrease the amount of oxalate absorbed into the body. However, blood oxalate levels were significantly lower in stone formers colonized with O. formigenes (1.70 µmol/l) than in those who were not colonized (5.79 µmol/l). The researchers theorized that rather than affecting oxalate absorption, O. formigenes degrades oxalate in the intestines thus increasing oxalate secretion from the intestinal cells into the intestines, lowering the blood oxalate levels and, hence, lowering urinary oxalate levels (24).
There is the possibility that people with high oxalate intakes can adapt by increasing the amount of oxalate degrading bacteria. A 2005 study from Germany, of only 4 people, indicated that over the course of six weeks, the percentage of oxalate absorbed is about the same as on a low-oxalate diet of 63 mg per day, about 7-10% (45). However, 10% of 600 mg is still about 10 times as high as 10% of 63 mg (6 vs. 60 mg absorbed). Two of these subjects tested positive for O. formigenese.
As of November 2013, there were no probiotic supplements with O. formigenes, though one company, OxThera, is in the process of creating one.
Liebman & Al-Wahsh reviewed the research on the probiotic supplements that have been tested to see if they reduce oxalate load (25). There were 6 studies, but they were fraught with different variables. Positive results were obtained by using the VSL#3 preparations from the company Oxadrop. Their current preparation (November, 2013) of VSL#3 contains:
- Bifidobacterium breve
- Bifidobacterium longum
- Bifidobacterium infantis
- Lactobacillus acidophilus
- Lactobacillus plantarum
- Lactobacillus paracasei
- Lactobacillus bulgaricus
- Streptococcus thermophilus
This preparation taken at a dose of 800 billion bacteria, once a day, dissolved in water after the last meal of the day for 4 weeks, reduced urinary oxalate excretion by 33% (27). A follow-up test compared a 450 billion dose of VSL#3 to a 900 billion and found better results with the 900 billion but it wasn’t statistically significant (28).
Decreasing Calcium-Oxalate Formation in the Kidney for Stone Prevention
Many studies have found that higher fluid intake is associated with a lower risk of kidney stones (see the section under calcium for a few such studies).
A 1996 case-control study from Italy compared 24-hour urinary fluid between stone-formers and matched controls (54). Male stone formers urinated an average of 1.06 L per day compared to 1.40 L from non-stone formers, while female stone-formers urinated an average of .99 L compared to 1.24 L in non-stone formers.
In fact, it might only take increasing fluid intake by about a liter (4.2 cups) per day to significantly reduce the chances of a second calcium-oxalate kidney stone. That same study from Italy took the stone-formers and divided them into two groups, those receiving no treatment other than increased fluid and those receiving no treatment at all. After 5 years, only 12 out of 99 had relapsed in the fluid group compared to 27 out of 100 in the untreated group. The fluid treatment group had raised their fluid output by about 1.0 to 1.5 L over the course of the five years. (54)
Hypocitraturia, which is low levels of citrate in the urine, increases the risk of kidney stones. Citrate combines with calcium in the kidneys to form a soluble complex resulting in less free calcium available to combine with oxalate (or phosphate).
Hypocitraturia is defined as < 320 mg (1.67 mmol) urinary citrate/day (62). However, a 24-hour urinary citrate concentration of ≥ 600 mg (3.12 mmol) is closer to the amount in healthy, non–stone forming individuals (62). Interventions to increase urinary citrate are a primary focus of the medical treatment of kidney stones (62), usually with potassium citrate.
Chronic diarrhea is thought to contribute to low urinary oxalate.
A 1986 cross-sectional study from the University of Chicago determined that the calcium to citrate ratio in the urine was the most important marker distinguishing the urine of people with kidney stones from those without, with higher ratios among the stone formers (32). Other markers that did not predict stone-formers as well included calcium alone, citrate alone, oxalate, sodium, and even the concentrated product ratio (CPR) which is a measure of calcium saturation.
A 2013 cross-sectional study from Spain had a similar finding (33). Kidney stone patients had low citrate levels in 32% of cases compared to 14% in the control group. They also found low urine citrate to be the best stone-related marker for predicting loss of bone mineral density. Oddly, they did not measure urinary oxalate levels.
Potassium citrate is a pharmaceutical used to treat kidney stones, especially in cases of hypocitraturia (34) or recurrent stones. In addition to lowering the rate of kidney stones, potassium citrate has been shown in two studies to increase bone mineral density in kidney stone formers (51, 57)
It is important to find out what type of kidney stone you have because treatment with potassium citrate can raise the urine pH which can exacerbate calcium-phosphate (aka brushite) kidney stones (especially if it gets above 7.0). Potassium-citrate treatment should only be taken under medical supervision.
Calcium citrate supplements are recommended for preventing calcium-oxalate stones by some experts. The University of Wisconsin-Madison Health and Nutrition Education handout for preventing oxalate kidney stones says, “While calcium carbonate and calcium citrate supplements are both useful for binding oxalate in the gastrointestinal tract, calcium citrate supplements are recommended as they seem to help kidneys excrete urinary citrate and decrease your risk for calcium stones (40).”
A 1994 study by Cornell University gave 1,000 mg of calcium, in the form of calcium citrate, to 14 women for 6 months as treatment for low bone mineral density in previous kidney stone formers (48). Participants were instructed to avoid high-oxalate foods and avoid excessive amounts of animal protein. After one month, urinary calcium and citrate increased. After six months, urinary calcium had dropped a bit compared to 1-month and parathyroid hormone and active vitamin D were significantly lower (indicating the body was no longer signaling the need for high calcium absorption). Calcium-oxalate supersaturation didn’t change significantly over the course of the study, though it was slightly lower at the end. Apparently, no participant developed a stone during the 6 months, though this was not explicitly stated, and, oddly, the paper did not report whether calcium citrate increased bone mineral density.
The authors believed that this study showed calcium citrate supplements to be safe for women with low bone mineral density who have had kidney stones, but cautioned that it was a small study and might not apply to women who are overweight or not adhering to a low-oxalate diet.
A 2004 study from the University of Texas Southwestern Medical Center tested potassium citrate, calcium citrate (400 mg of calcium twice a day), and a combination of each for 2 weeks on women who were not stone formers (50). Calcium citrate lowered oxalate excretion while potassium citrate lowered calcium-oxalate saturation.
As of December 2013, there were not many calcium citrate supplements that do not contain vitamin D3 as cholecalciferol which is not vegan. However, there are some pure calcium citrate powders on the market:
Because potassium citrate can have some side effects and comes in large tablets that are inconvenient to take, researchers have studied various beverages to see if there are any that could replace potassium citrate treatment. Orange juice was a candidate because it is high both in potassium and citrate, though it also contains some oxalate and vitamin C.
The research, which is summarized below, indicates that orange juice and lemon juice (or lemonade) can decrease the risk for stones, though about 6 g per day of citrate is necessary. See the table below for citrate amounts. Grapefruit juice and cranberry juice are most likely neutral.
Beverages and Stone Occurrence
In 2013, following up on the earlier work in their cohorts (61), Harvard School of Public Health compared those drinking from < 1 serving/week to > 1 serving/day of many beverages. The occurrence of kidney stones were affected in the following ways (60):
- Decreased – coffee, decaffeinated coffee, tea, red wine, white wine, beer, orange juice
- No effect – artificially sweetened cola, artificially sweetened noncola soda, liquor, apple juice, grapefruit juice, tomato juice, whole milk, skim milk, water
- Increased – sugar-sweetened cola, sugar-sweetened noncola soda, punch
A 2007 study from Duke University found that daily treatment with 120 ml of concentrated lemon juice mixed with 2 liters of water (5.9 g of citric acid total) raised urinary citrate from 350 to 733 mg per day (67). The lemonade treatment reduced stone incidence from 1.0 to .13 stones per person per year. There was a control group receiving potassium-citrate therapy, but the stone incidence was not measured for them.
Beverages and Stone Markers
A 2006 study from the University of Texas Southwestern Medical Center found that 2.1 g of citrate, 3 times per day, of orange juice almost doubled urinary citrate while 2.1 g of citrate from lemonade had no impact (11).
A 1994 study from the University of Texas Southwestern compared one week of placebo, potassium citrate, and orange juice in participants with a history of hypocitraturia and kidney stones and participants with no history (74). Each participant went through all three treatments. The results were similar in both stone formers and non-stone formers, so they combined the results. The orange juice provided 11.6 g of citrate per day. They did not compare baseline levels to treatment levels. Both potassium-citrate and orange juice treatment increased citrate more than the placebo and about the same amount (to about 950 mg per day). Orange juice treatment raised urinary oxalate compared to the other two groups (26 mg to 34 mg per day). However, calcium intake on these diets was kept low at 400 mg per day; on a normal calcium diet, oxalate might not increase. The authors thought perhaps the small amounts of oxalate in orange juice, the carbohydrate, or the vitamin C might have contributed to the higher oxalate levels.
A 2007 study from the University of Wisconsin found that 4 oz of lemon juice or 32 oz of lemonade per day (they assumed each contained 5.9 g) increased urinary citrate levels of patients who had experienced kidney stones from 683 mg/day to 886 mg/day (65). Another group was treated with the lemon therapy and also potassium citrate and increased their citrate levels from 364 mg/day to 700 mg/day.
A 2007 study from Walter Reed Army Medical Center found that 4.5 g of citrate in lemonade, spread over 3 doses per day, barely raised citrate levels from 263 to 309 mg/day (66).
A 1996 study for University of California San Francisco gave lemonade to stone formers with hypocitraturia containing 5.9 g of citric acid per day (73). Urinary citrate increased significantly from 142 to 346 mg per day. Urinary oxalate decreased from 53 to 43 mg per day.
A 2003 study from Germany found that grapefruit, apple, and orange juice only slightly raised citrate levels (70). However, the participants did not have hypocitraturia and were not stone formers. Only grapefruit juice succeeded in reducing calcium-oxalate saturation to a statistically significant degree, though the other juices reduced it slightly.
A 2002 study from Italy found that grapefruit juice diluted to 10% with mineral water (to provide 2.1 g of citrate) slightly increased hourly urine citrate levels (71). When compared to mineral water only, the diluted grapefruit juice raised urine citrate levels a statistically significant amount, but that was because the mineral water-only treatment actually reduced citrate levels.
A 2001 study from the New York Veterans Affairs Medical Center tested 3 doses of 240 ml (about a cup) per day of grapefruit juice on non-stone formers (72). Urinary citrate and potassium levels increased, but so did oxalate. The researchers did a test to determine that the oxalate did not come from vitamin C (in the kidneys, anyway). Calcium-oxalate saturation increased slightly, but not to a significant degree on the grapefruit juice treatment.
A 2005 study from University of Texas Southwestern Medical Center tested cranberry juice (53). They gave stone and non-stone formers 2.3 g of citrate per day in 1 liter of cranberry juice broken into two doses. Urinary citrate actually decreased from 490 to 470 mg/day in stone formers. It also decreased in non-stone formers. The cranberry juice had a positive effect on markers of uric acid stones but not for calcium-oxalate stones. They reported that one other study showed an increase (68) and one showed no change in citrate excretion using cranberry juice (69). It seems safe to conclude that cranberry juice should not be the beverage of choice in preventing calcium-oxalate kidney stones or correcting hypocitraturia.
Table 2 shows the amount of citrate in various beverages as measured by researchers at the University of Wisconsin (62), and Duke University and Brown University (63). Various brands of lemonade and limeade were all lower.
|Table 3. Citrate in Beverages (g per Cup)|
|Grapefruit juice – ready-to-consume||5.91||400||62|
|Grapefruit juice – ready-to-consume||2.89||400||63|
|Lemon juice – fresh||2.13||251||63|
|Lemon juice – fresh||11.36||251||62|
|Lemon juice – from concentrate||8.67||217||62|
|Lemonade – homemade||0.78||42||63|
|Lime juice – fresh||10.84||283||62|
|Lime juice – from concentrate||8.38||62|
|Orange juice – fresh||2.15||496||62|
|Orange juice – ready-to-consume||3.97||443||62|
Restricting sodium might help prevent calcium-oxalate stones. A calcium atom is typically excreted with each sodium atom, so if you are urinating a lot of sodium, your urine is going to contain more calcium (other things being equal), providing a chance for calcium to bind with oxalate.
To my knowledge, there are no clinical trials using sodium restriction as the main treatment to prevent kidney stone recurrence, though one trial from Italy found that reducing sodium intake from 5,244 mg to 1,564 g per day decreased urinary calcium and oxalate (39).
Theoretically, oxalate should be able to bind to plant iron, especially when iron is in the ferrous (Fe2+) state and prevent its absorption. There has not been much research. A 2008 study from Switzerland examined iron absorption from bread in meals containing spinach or kale with a whopping amount of 1,260 mg of added oxalate. They concluded that oxalate does not inhibit iron absorption (29).
Oxalate Content of Foods
The amount of oxalate in foods is hard to pin down. In a 2007 review of oxalate in the Journal of the American Dietetic Association, Massey reports that the part of the plant (stem vs. leaf, bran vs. endosperm), genetic differences between plant cultivars, soil conditions, and time of year harvested can account for differences in oxalate amounts (30). Massey noted that “[T]he differences in oxalate content of the final food due to modification of cultivation conditions are usually quite modest compared to the oxalate differences in cultivars. Therefore, breeding of commercially viable low oxalate cultivars seems a more promising approach to reducing oxalate in foods.”
As described in the section on Soluble vs. Insoluble, the cooking method can also make a big difference in foods with a high content of soluble oxalate (which might be the only type that is absorbed at a significant rate in most people). Boiling or steaming and discarding the water can reduce the amount of oxalate, especially in the leaves of leafy greens.
Please see the table Calcium and Oxalate Content of Foods for the oxalate amounts in foods reported in the scientific literature or by the USDA. Unfortunately, there are many foods which are not included and there is much talk in the low-oxalate community suggesting the “old” methods of testing oxalate amounts in foods is inaccurate. I’m working on sorting this out.
In the meantime, here are two alternative tables which list more foods:
- Oxalate Content of Foods.xls – downloadable Excel sheet from Harvard University published in 2007.
- Trying Low-Oxalate Yahoo Group – connected with LowOxalate.info website; if you join the group you can get access to their list of the oxalate content of foods.
- LowOxalate.info – website of Susan Owens, active in the low-oxalate community.
- Oxalosis and Hyperoxaluria Foundation
- LowOxalateInfo.com – website of Heidi Stallman; provides many low-oxalate recipes and other helpful links.
5. Terribile M, Capuano M, Cangiano G, Carnovale V, Ferrara P, Petrarulo M, Marangella M. Factors increasing the risk for stone formation in adult patients with cystic fibrosis. Nephrol Dial Transplant. 2006 Jul;21(7):1870-5. Abstract.
7. Konstantynowicz J, Porowski T, Zoch-Zwierz W, Wasilewska J, Kadziela-Olech H, Kulak W, Owens SC, Piotrowska-Jastrzebska J, Kaczmarski M. A potential pathogenic role of oxalate in autism. Eur J Paediatr Neurol. 2012 Sep;16(5):485-91.
16. Robertson WG, Peacock M, Heyburn PJ, Hanes FA, Rutherford A, Clementson E, Swaminathan R, Clark PB. Should recurrent calcium oxalate stone formers become vegetarians? Br J Urol. 1979 Dec;51(6):427-31.
20. Lange JN, Wood KD, Wong H, Otto R, Mufarrij PW, Knight J, Akpinar H, Holmes RP, Assimos DG. Sensitivity of human strains of Oxalobacter formigenes to commonly prescribed antibiotics. Urology. 2012 Jun;79(6):1286-9.
21. Kharlamb V, Schelker J, Francois F, Jiang J, Holmes RP, Goldfarb DS. Oral antibiotic treatment of Helicobacter pylori leads to persistently reduced intestinal colonization rates with Oxalobacter formigenes. J Endourol. 2011 Nov;25(11):1781-5.
22. Kaufman DW, Kelly JP, Curhan GC, Anderson TE, Dretler SP, Preminger GM, Cave DR. Oxalobacter formigenes may reduce the risk of calcium oxalate kidney stones. J Am Soc Nephrol. 2008 Jun;19(6):1197-203.
23. Jiang J, Knight J, Easter LH, Neiberg R, Holmes RP, Assimos DG. Impact of dietary calcium and oxalate, and Oxalobacter formigenes colonization on urinary oxalate excretion. J Urol. 2011 Jul;186(1):135-9.
24. Siener R, Bangen U, Sidhu H, Hönow R, von Unruh G, Hesse A. The role of Oxalobacter formigenes colonization in calcium oxalate stone disease. Kidney Int. 2013 Jun;83(6):1144-9. doi: 10.1038/ki.2013.104.
26. Turroni S, Bendazzoli C, Dipalo SC, Candela M, Vitali B, Gotti R, Brigidi P. Oxalate-degrading activity in Bifidobacterium animalis subsp. lactis: impact of acidic conditions on the transcriptional levels of the oxalyl coenzyme A (CoA) decarboxylase and formyl-CoA transferase genes. Appl Environ Microbiol. 2010 Aug;76(16):5609-20. doi: 10.1128/AEM.00844-10.
29. genannt Bonsmann SS, Walczyk T, Renggli S, Hurrell RF. Oxalic acid does not influence nonhaem iron absorption in humans: a comparison of kale and spinach meals. Eur J Clin Nutr. 2008 Mar;62(3):336-41.
31. There were 363 cases of kidney stones in 105,806 person-years. Assuming 50 adult years per person, this would be a 17% risk of getting a stone overall. A relative risk of 1.22 would put increase the risk from 17% to about 21%.
33. Arrabal-Polo MA, Arrabal-Martin M, Arias-Santiago S, Garrido-Gomez J, Poyatos-Andujar A, Zuluaga-Gomez A. Importance of citrate and the calcium : citrate ratio in patients with calcium renal lithiasis and severe lithogenesis. BJU Int. 2013 Apr;111(4):622-7.
34. Ettinger B, Pak CY, Citron JT, Thomas C, Adams-Huet B, Vangessel A. Potassium-magnesium citrate is an effective prophylaxis against recurrent calcium oxalate nephrolithiasis. J Urol. 1997 Dec;158(6):2069-73.
37. Curhan GC, Willett WC, Speizer FE, Spiegelman D, Stampfer MJ. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Intern Med. 1997 Apr 1;126(7):497-504.
39. Nouvenne A, Meschi T, Prati B, Guerra A, Allegri F, Vezzoli G, Soldati L, Gambaro G, Maggiore U, Borghi L. Effects of a low-salt diet on idiopathic hypercalciuria in calcium-oxalate stone formers: a 3-mo randomized controlled trial. Am J Clin Nutr. 2010 Mar;91(3):565-70.
40. Olson N, Van Riet S, Penniston K. utrition Tips to Treat and Prevent Calcium Oxalate Kidney Stones. University of Wisconsin-Madison Health and Nutrition Education. Revised 3/2010. (PDF) Accessed October 2013.
42. Hueppelshaeuser R, von Unruh GE, Habbig S, Beck BB, Buderus S, Hesse A, Hoppe B. Enteric hyperoxaluria, recurrent urolithiasis, and systemic oxalosis in patients with Crohn’s disease. Pediatr Nephrol. 2012 Jul;27(7):1103-9.
48. Levine BS, Rodman JS, Wienerman S, Bockman RS, Lane JM, Chapman DS. Effect of calcium citrate supplementation on urinary calcium oxalate saturation in female stone formers: implications for prevention of osteoporosis. Am J Clin Nutr. 1994 Oct;60(4):592-6.
52. Emmett M, Guirl MJ, Santa Ana CA, Porter JL, Neimark S, Hofmann AF, Fordtran JS. Conjugated bile acid replacement therapy reduces urinary oxalate excretion in short bowel syndrome. Am J Kidney Dis. 2003 Jan;41(1):230-7.
54. Borghi L, Meschi T, Amato F, Briganti A, Novarini A, Giannini A. Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study. J Urol. 1996 Mar;155(3):839-43.
56. Voss S, Hesse A, Zimmermann DJ, Sauerbruch T, von Unruh GE. Intestinal oxalate absorption is higher in idiopathic calcium oxalate stone formers than in healthy controls: measurements with the [(13)C2]oxalate absorption test. J Urol. 2006 May;175(5):1711-5.
57. Vescini F, Buffa A, La Manna G, Ciavatti A, Rizzoli E, Bottura A, Stefoni S, Caudarella R. Long-term potassium citrate therapy and bone mineral density in idiopathic calcium stone formers. J Endocrinol Invest. 2005 Mar;28(3):218-22.
58. Caudarella R, Vescini F, Buffa A, Sinicropi G, Rizzoli E, La Manna G, Stefoni S. Bone mass loss in calcium stone disease: focus on hypercalciuria and metabolic factors. J Nephrol. 2003 Mar-Apr;16(2):260-6.
62. Penniston KL, Nakada SY, Holmes RP, Assimos DG. Quantitative assessment of citric acid in lemon juice, lime juice, and commercially-available fruit juice products. J Endourol. 2008 Mar;22(3):567-70.
63. Haleblian GE, Leitao VA, Pierre SA, Robinson MR, Albala DM, Ribeiro AA, Preminger GM. Assessment of citrate concentrations in citrus fruit-based juices and beverages: implications for management of hypocitraturic nephrolithiasis. J Endourol. 2008 Jun;22(6):1359-66.
66. Koff SG, Paquette EL, Cullen J, Gancarczyk KK, Tucciarone PR, Schenkman NS. Comparison between lemonade and potassium citrate and impact on urine pH and 24-hour urine parameters in patients with kidney stone formation. Urology. 2007 Jun;69(6):1013-6.
67. Kang DE, Sur RL, Haleblian GE, Fitzsimons NJ, Borawski KM, Preminger GM. Long-term lemonade based dietary manipulation in patients with hypocitraturic nephrolithiasis. J Urol. 2007 Apr;177(4):1358-62.
70. Hönow R, Laube N, Schneider A, Kessler T, Hesse A. Influence of grapefruit-, orange- and apple-juice consumption on urinary variables and risk of crystallization. Br J Nutr. 2003 Aug;90(2):295-300.
71. Trinchieri A, Lizzano R, Bernardini P, Nicola M, Pozzoni F, Romano AL, Serrago MP, Confalanieri S. Effect of acute load of grapefruit juice on urinary excretion of citrate and urinary risk factors for renal stone formation. Dig Liver Dis. 2002 Sep;34 Suppl 2:S160-3.
77. Turney BW, Appleby PN, Reynard JM, Noble JG, Key TJ, Allen NE. Diet and risk of kidney stones in the Oxford cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC). Eur J Epidemiol. 2014 Apr 22. [Epub ahead of print]
Allie-Hamdulay S, Rodgers AL. Prophylactic and therapeutic properties of a sodium citrate preparation in the management of calcium oxalate urolithiasis: randomized, placebo-controlled trial. Urol Res. 2005 May;33(2):116-24. Abstract.
Borghi L, Schianchi T, Meschi T, Guerra A, Allegri F, Maggiore U, Novarini A. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med. 2002 Jan 10;346(2):77-84.
Clinical trial in which low-calcium diet increased risk of kidney stones.
Ramsubeik K, Keuler NS, Davis LA, Hansen KE. Factors Associated with Calcium Absorption in Postmenopausal Women: A Post Hoc Analysis of Dual-Isotope Studies. J Acad Nutr Diet. 2013 Oct 24. doi:pii: S2212-2672(13)01278-1. 10.1016/j.jand.2013.07.041. [Epub ahead of print]
Dietary fat has consistently been associated with higher calcium absorption. Authors suggest possibly due to higher estradiol levels.
In female patients with recurring urinary tract infections (who had been treated with antibiotics), urinary oxalate excretion was significantly higher (0.374 mmol/day) than in women without urinary tract infections (0.308 mmol/day) (P < 0.05).