Kidney Stones

Kidney Stones

Last updated: 08/2020

Contributor(s): Dr. Maureen Williams, ND

1 Overview

Summary and Quick Facts

  • Kidney stones are hard masses that form in one or both kidneys. Kidney stones can be extremely painful, can recur whether treated or not and increase risk for decreased kidney function and chronic kidney disease.
  • This protocol details how kidney stones form. You will also learn about treatment options for kidney stones, which depend primarily on the type of stone, and dietary and lifestyle strategies that can reduce risk, such as increasing fluid intake.
  • While calcium was once thought to contribute to kidney stone risk, studies have shown it can, in fact, decrease risk.

Kidney stones form when compounds in the urine gather into a solid mass. They can cause extreme pain and urinary blockage. There are different types of stones, with some of the most common being calcium oxalate, calcium phosphate, and uric acid stones. Kidney stone formers are at twice the risk for developing decreased kidney function and chronic kidney disease compared with non-formers.

Magnesium and calcium, particularly in their citrate forms; vitamin B6; and probiotics may help prevent kidney stones.

Causes and Risk Factors

  • Dehydration is an important risk factor for all types of kidney stones.
  • Urine composition, such as pH, excessive calcium, oxalates, or uric acid in the urine are associated with kidney stone risk.
  • Animal protein intake can increase the risk of kidney stones.

Note: It was assumed that calcium intake, from diet or supplements, contributed to kidney stone risk. However, low calcium intake is now known to increase kidney stone risk.

Signs and Symptoms

  • Kidney stones can be present in the kidney without causing symptoms, sometimes for years.
  • The hallmark symptom of a kidney stone is sudden, severe flank pain that is usually one-sided.


  • A patient’s history, physical exam, and urinalysis often clearly indicate acute kidney stones.
  • Kidney stones are sometimes found during diagnostic imaging that is being performed for another reason.

Conventional Treatment

  • All kidney stones have their composition analyzed and a 24-hour urine analysis is performed for both diagnosis and prevention.
  • Pain management is often accomplished with nonnarcotic or narcotic pain relievers and NSAIDs.
  • Lithotripsy uses shock waves to break the kidney stone into smaller fragments.
  • Preventive treatment may include allopurinol or thiazide diuretics.

Novel and Emerging Strategies

  • Bisphosphonates can help keep urine calcium concentrations from rising by reducing bone breakdown and calcium loss.
  • Sleep position may predict the side on which kidney stones will occur, as a study showed 76% of kidney stone formers slept on the same side as their stones.
  • Oxalobacter formigenes, bacteria found in the digestive tract, prevented calcium oxalate kidney stones in clinical studies. This probiotic is currently available only as a pharmaceutical, not as a dietary supplement.

Dietary and Lifestyle Considerations

  • Increase fluid intake, especially citrus juices and mineral water.
  • Eat more fruits and vegetables, as they are protective against most types of kidney stones.
  • Reduce dietary purines (including organ meats and seafood) and dietary oxalates (including spinach and French fries).

Integrative Interventions

  • Magnesium: Higher magnesium consumption, and especially magnesium citrate, is significantly associated with lower risk of calcium oxalate kidney stones. In order to bind dietary oxalate, magnesium must be taken at the same time as oxalate-containing foods.
  • Calcium: High dietary calcium has been shown to decrease kidney stone risk. Taken in its citrate form, calcium can help alkalinize urine and reduce the rate of stone formation.
  • Probiotics: Certain Lactobacillus and Bifidobacteria strains may reduce urinary oxalate and decrease kidney stone risk, especially in people with high urinary oxalate concentrations.
  • Vitamin B6: In a 14-year study in women, kidney stone risk was 34% lower in those who consumed the most vitamin B6 per day from diet and supplements compared with those who consumed the least.
  • Fish oil: Fifteen healthy people were given EPA and DHA for 30 days; excessive urinary oxalate excretion and calcium oxalate saturation was decreased at the end of the trial.

2 Introduction

Kidney stones form when compounds in the urine aggregate into a solid mass (Aggarwal 2013). Kidney stones can cause extreme pain and urinary blockage in severe cases (UMMC 2013).

About 7% of women and 13% of men in the United States will have at least one bout of kidney stones requiring medical attention in their lifetime (Aliotta 2015). Unfortunately, kidney stones have a high rate of recurrence: without treatment, the risk of a second episode of kidney stones is as high as 50% during the seven years following the first occurrence (Xu 2013). Thus, taking steps to reduce kidney stone risk after a first episode is of the utmost importance.

Increasing fluid intake is one of the most effective ways to prevent kidney stones, since greater urine volume decreases the concentration of stone-forming compounds. Dietary habits such as increasing fruit and vegetable intake and decreasing intake of animal protein may play a role in reducing susceptibility to some types of kidney stones, since the foods we eat influence the composition of our urine (Heilberg 2013).

One important consideration for kidney stone formers is often overlooked: people who have a history of kidney stones may be more susceptible to chronic kidney disease. In fact, the association between kidney stones and chronic kidney disease is independent of major kidney disease risk factors like high blood pressure and diabetes: stone formers are at twice the risk for developing decreased kidney function and chronic kidney disease compared with non-formers (Keddis 2013; Frassetto 2011).

Generally, small kidney stones will pass with no medical intervention other than pain management and hydration. Doctors sometimes prescribe medications to relax the ureters and ease the passage of the stones. Larger stones, and stones that fail to pass or cause especially severe pain or obstruction and infection may require more aggressive therapies such as antibiotics, lithotripsy (therapy utilizing ultrasound shock waves to break stones into smaller fragments), or surgery to remove stones (Antonelli 2015).

A fundamental aspect of kidney stone management is analyzing the chemical composition of the patient’s urine and kidney stones (if available). Different stone types require different treatments. A 24-hour urine profile is a useful tool in determining the type of stone(s) a patient has or is prone to developing (LabCorp 2015). Calcium oxalate, calcium phosphate, and uric acid stones are the most prevalent, and these differ in their causes and treatments. For instance, calcium oxalate and uric acid stones are best addressed by raising urine pH while calcium phosphate stones require lowering urine pH (Xu 2013; Sakhaee, Maalouf 2012; Healy 2012; Curhan 2012; Coe 2015).

Several natural interventions may help prevent certain types of stone formation. For example, supplemental magnesium and calcium, particularly in their citrate forms; vitamin B6; and probiotics may help prevent calcium oxalate stones, the most common type of kidney stones (Negri 2013; Zimmermann 2005; Taylor 2004; Caudarella 2009; del Valle 2013; Sakhaee 2004; Ettinger 1997; Ferraz 2009; Curhan 1999).

Not long ago, it was assumed that calcium intake, from diet or supplements, contributed to kidney stone risk. Some physicians even went as far as telling kidney stone patients to restrict calcium intake. But this theory has been disproven, and low calcium intake is now known to increase kidney stone risk. Calcium supplementation was not associated with kidney stone risk in a rigorous analysis of data from 10 studies (Martini 2002; Candelas 2012). 

In this protocol you will learn about the different types of kidney stones and how they form. Factors that increase kidney stone risk will be described, and little known connections between kidney stones and several chronic health conditions will be reviewed. You will also learn about how kidney stones are typically treated, and ways to reduce kidney stone risk with dietary strategies and natural interventions.

Given the underappreciated connection between kidney stones and chronic kidney disease, readers of this protocol should also review Life Extension’s Kidney Health and Chronic Kidney Disease protocols, which describe more general strategies for preserving kidney health.

3 Background

The Urinary Tract

The kidneys maintain the necessary balance of electrolytes and fluids in the bloodstream by filtering all of the blood in the body through microscopic structures called nephrons. Nephrons allow water and some waste products to enter the urine, while retaining cells and large molecules in the blood (NIDDK 2014). The kidneys also help maintain a slightly alkaline blood pH (between 7.37 and 7.43) by excreting excess acid or base (Koeppen 2009; Lewis 2013).

The final product of this filtration process, urine, is collected from the nephrons and eventually drains into narrow tubes called ureters that connect the kidneys to the bladder. Finally, urine leaves the bladder and the body via another narrow tube called the urethra (NIH 2014).

How Kidney Stones Form

Urine becomes more concentrated as it moves through the kidneys and as water is reabsorbed into the bloodstream (Sands 2009). Minerals and organic molecules that are dissolved in the urine can crystallize if the urine becomes highly concentrated. These crystals can stick together and form complexes with other molecules, particularly proteins. These crystalline-protein complexes are the main components of kidney stones (Aggarwal 2013; UMMC 2014).

There are five major types of kidney stones (Aliotta 2015; Preminger 2015; Antonelli 2015):

  • Calcium oxalate. From 60‒80% of all kidney stones are entirely calcium oxalate or predominantly calcium oxalate with a smaller percentage of calcium phosphate.
  • Calcium phosphate. Pure calcium phosphate stones are less common, accounting for 10‒20% of all kidney stones.
  • Uric acid. Uric acid stones account for up to 20% of all kidney stones.
  • Struvite. Kidney stones are made of struvite, which is magnesium ammonium phosphate, in 1‒7% of cases. Struvite stones are associated with chronic urinary tract infections involving certain types of bacteria, and are up to three times more common in women.
  • Cystine. Stones made of the amino acid cystine are rare in adults and more common in children, representing 1‒3% of all kidney stone cases.

Very small stones can pass through the entire urinary tract without causing symptoms, but larger stones can become lodged in the ureters, bladder, or urethra (NLM 2015; Johns Hopkins 2015). Stones that become lodged in the urinary tract can cause severe pain and block urine flow (UMMC 2013; Singh 2011). Kidney stones are frequently passed without complications, using only conservative treatment such as pain relief and hydration (Aliotta 2015; Antonelli 2015).

Kidney Stones and Chronic Kidney Disease

Kidney stones increase the risk of chronic kidney disease and end-stage renal disease (Frassetto 2011), independently of risk factors shared by stone formers and those with chronic kidney disease such as high blood pressure and diabetes. It is estimated that the risk of chronic kidney disease is twice as high in stone formers compared with non-stone formers (Keddis 2013).

This relationship may be related to stone size and number. In one study, greater cumulative stone size was associated with higher chronic kidney disease risk, suggesting people who either form large stones or many smaller stones are at greater risk (Ahmadi 2015).

Some researchers have proposed that the presence of crystals and stones in kidney tissues can trigger chronic inflammatory processes and scarring that directly contribute to chronic kidney dysfunction and disease (Keddis 2013; Aggarwal 2013).

Given the link between history of kidney stones and chronic kidney disease, individuals who are stone formers should also review the protocol on Kidney Health, which describes many strategies for keeping the kidneys healthy.

4 Causes and Risk Factors


One of the most important risk factors for all types of kidney stones is dehydration (Wong 2015; Curhan 2012; Antonelli 2015). When there is too little water in the urine, stone-forming molecules are more concentrated and more likely to form crystals (Aggarwal 2013). In general, a urine flow rate of less than 1 L per day increases the risk of stone formation (Curhan 2012), and guidelines for people with a history of kidney stones include the recommendation to maintain their urine output above 2 L per day (Antonelli 2015).

Urine Composition

In addition to the concentration or diluteness of the urine, other urinary factors are associated with kidney stone risk (Sakhaee, Maalouf 2012).

Urine pH. The pH of urine is largely determined by diet (Adeva 2011). For example, a diet high in animal protein tends to promote acidic conditions and lower urine pH (Fenton 2011; Friedlander 2015; Schwalfenberg 2012). The most common types of kidney stones, calcium oxalate and uric acid, usually form in acidic urine—as do cystine stones, which are uncommon. On the other hand, urine alkalinity may increase the risk of calcium phosphate and struvite stones (Frassetto 2011). Since varying urine composition and pH can give rise to different types of stones, it is critical that patients undergo urine analysis and have their stone type determined before treatment is initiated. Different types of stones require different treatment approaches (UCKSETP 2015).

Hypercalciuria. Hypercalciuria is excessive calcium in the urine; sometimes this occurs even when calcium intake is not excessive and blood calcium level is normal (Chines 1995). Hypercalciuria may be related to problems in the digestive tract that lead to increased calcium absorption, or dysfunctional renal calcium handling, but often no underlying cause is identified (Aliotta 2015). Excess urine calcium increases the risk of calcium oxalate and calcium phosphate kidney stones (Escribano 2014).

Hyperoxaluria. Hyperoxaluria refers to high oxalate concentration in the urine and is seen in 10‒40% of people with calcium oxalate stones, though it can also be present in individuals without kidney stone disease (Curhan 2012). One important determinant of the amount of oxalate in the urine is the amount absorbed from the intestines from food (Xu 2013). High oxalate concentrations are present in several foods, including nuts and nut butters and some vegetables and fruits, and can be made in the body from other compounds including vitamin C (Pena de la Vega 2004; UMICH 2015). Vitamin C supplementation has been shown to increase urinary oxalate in people with a history of kidney stones (Baxmann 2003; Urivetzky 1992), and some observational studies have identified associations between vitamin C supplementation and increased kidney stone risk, primarily in men (Thomas 2013; Ferraro 2016). Although vitamin C supplementation has not been shown to cause kidney stones in randomized controlled trials, it may nevertheless be prudent for people with a history of calcium oxalate kidney stones to consult a qualified healthcare provider before initiating supplementation with high-dose vitamin C.

Hypocitraturia. Hypocitraturia is too little citrate in the urine. Citrate is an alkalinizing molecule that raises urine pH, binds calcium in the urine, and blocks calcium oxalate and calcium phosphate crystallization. Thus, urinary citrate protects against calcium oxalate and uric acid kidney stones. Low intake of dietary citrate from vegetables and fruits and high animal protein intake may contribute to hypocitraturia, though often the cause is unknown (Curhan 2012; Zuckerman 2009; Pak 1986).

Hyperuricosuria. Hyperuricosuria is excessive uric acid concentration in the urine, which increases the risk of uric acid and calcium oxalate kidney stones. Hyperuricosuria commonly occurs in gout, but has many other possible causes, such as certain medications or excess purine intake (purines are organic compounds common in organ meats, some fish, and beer) (Zwolinska 2000; Ngo 2007; Halabe 1994; Maalouf 2011). Uric acid stones are more common in people with metabolic syndrome and in those with gout. About 20% of people with gout develop uric acid kidney stones (Grassi 2011; Xu 2013).

Dietary Risk Factors

High salt intake. A high-salt diet contributes to kidney stone risk, at least in part, because high sodium intake raises urine calcium concentration (Sakhaee, Maalouf 2012; Friedlander 2015).

High sugar intake. A high-sugar diet appears to raise the risk of kidney stones, which may relate in part to the ability of refined sugar and large quantities of carbohydrate to elevate urine calcium (Thom 1978; Garg 1990). In a 12-year study of 91 731 women, those who ate the most refined sugar were 52% more likely to develop kidney stones than those who ate the least (Curhan 1997). Similarly, in a study of nearly 200 000 individuals over an average of eight years, those who consumed the most sugar-sweetened soft drinks were 23% more likely to develop kidney stones compared with those who consumed the least (Ferraro 2013).

Low calcium intake. Although dietary calcium restriction was previously thought to lower urine calcium and calcium-containing stone risk, evidence from multiple large observational studies and a randomized controlled trial has shown that calcium restriction does not prevent stone formation (Friedlander 2015). In fact, calcium actually binds to oxalate in the digestive tract, preventing oxalate from entering the bloodstream. This then lowers urinary oxalate, and may help prevent calcium oxalate kidney stones. This possibility has received support from epidemiologic studies that have found that lower dietary calcium intake actually increases kidney stone risk (Sakhaee, Maalouf 2012; Sorensen, Eisner 2012).

Low fruit and vegetable intake. Several fruits and vegetables provide alkaline-forming substances including bicarbonate, citrate, and potassium, which alkalinize urine, reduce urinary calcium excretion, and raise urinary citrate, thus reducing kidney stone risk (Morris 1999).

Animal Protein Intake and Kidney Stones

Animal protein acidifies urine, decreases urinary citrate, and raises urinary calcium and uric acid, potentially increasing risk of calcium and uric acid kidney stones (Friedlander 2015; Gul 2014; Lambert 2012).

A small randomized study in healthy individuals found that beef, chicken, and fish have similar potential to promote kidney stone formation based on their impact on urinary uric acid and urine chemistry (Tracy 2014). Overall, vegetarians have a lower risk of stone development than meat eaters; and among meat eaters, studies suggest those who consume more fruits and vegetables are less likely to form kidney stones (Espinosa 2012).

The effectiveness of a diet low in animal protein, independent of other dietary changes, for preventing kidney stones has yet to be rigorously studied (Friedlander 2015), but several expert sources recommend restriction of animal protein in order to reduce the risk of calcium oxalate stone formation and recurrence (Curhan 2012; Trinchieri 2013; Heilberg 2013; UMMC 2013).


Some medications can affect urine chemistry and increase the likelihood of kidney stone formation. In general, these medications cause higher urinary levels of calcium, uric acid, or oxalate. Examples of such medications include (Antonelli 2015; Husain 2012):

  • A class of antiviral drugs known as protease inhibitors
  • A class of drugs known as carbonic anhydrase inhibitors, which includes some drugs used to treat glaucoma, epilepsy, and edema
  • The decongestant ephedrine and the expectorant guaifenesin (Mucinex, Robitussin)
  • Some diuretics such as triamterene (Dyrenium)
  • The antibiotic sulfadiazine

Conditions Associated with Increased Kidney Stone Risk

Impaired kidney function. Kidney diseases and disorders that impair renal calcium handling cause high urinary calcium and thereby increase stone risk. Similarly, kidney diseases that cause increased phosphate in the urine also contribute to stone risk (Arrabal-Polo, Arrabal-Martin 2013; Aliotta 2015).

Hyperparathyroidism. In this condition, parathyroid hormone levels are elevated. This leads to increased intestinal calcium absorption and calcium removal from bones, raising blood calcium levels as well as urine calcium concentrations and kidney stone risk (Gasser 2013; Nussey 2001; Moe 2008). 

Osteoporosis. Emerging evidence suggests a strong relationship between bone loss and kidney stones. This has led some researchers to recommend osteoporosis testing for recurrent kidney stone formers (Arrabal-Polo, Sierra Giron-Prieto 2013).

Digestive and intestinal disorders. People with chronic diarrhea or inflammatory bowel diseases like ulcerative colitis and Crohn’s disease absorb more dietary oxalate, leading to hyperoxaluria and thus an increased calcium oxalate stone risk (Aliotta 2015). Hyperoxaluria can also occur in people with fat malabsorption due to digestive disorders or after gastrointestinal surgery, including bariatric surgery for weight loss. In this condition, excess (unabsorbed) fat in the gut binds to calcium, which then cannot attach to and block absorption of oxalate (Arrabal-Polo, Arrabal-Martin 2013; Nazzal 2015).

Type 2 diabetes. People with diabetes have more acidic urine and higher urinary uric acid and oxalate than people without diabetes, increasing their risk of uric acid and calcium oxalate kidney stones (Eisner 2010; Torricelli 2014; Hartman 2015).

Kidney stones, insulin resistance, and metabolic syndrome. The American Heart Association defines metabolic syndrome by the presence of three or more of the following risk factors: abdominal obesity, high blood pressure, elevated fasting glucose, high triglycerides, and low HDL cholesterol. Metabolic syndrome is associated with increased kidney stone risk (Sakhaee 2008; Wong 2015; Kaur 2014; AHA 2014).

Insulin resistance, a central feature of impaired glucose metabolism and metabolic syndrome, may partly explain the link, because it increases urine acidity and has been associated with uric acid stone formation (Ahmed 2014). In fact, the American Urologic Association suggests people with recurrent uric acid kidney stones should be screened for insulin resistance and metabolic syndrome (Li 2014). 

Risk Factors for Uncommon Stones

Cystinuria. Cystine stones occur only in people with a genetic condition called cystinuria, in which the kidneys excrete a large amount of cystine, an amino acid that has a high tendency to form stones (Xu 2013).

Infection. Certain urinary tract infections increase the risk of struvite stones. These infections involve a type of bacteria known as urease-producing (or urea-splitting) bacteria. Some examples of urease-producing bacteria are Klebsiella, Proteus, Pseudomonas, and Enterococcus species. These bacteria can colonize the kidneys and increase risk of struvite precipitation, leading to stone formation (Xu 2013). Struvite stones are more common in women than men; infants and the elderly also have increased susceptibility (Curhan 2012; Kristensen 1987; Gettman 1999).

5 Signs and Symptoms

Kidney stones can be present in the kidney without causing symptoms for months, years, and sometimes decades (Curhan 2012). Symptoms usually occur as a result of a stone moving into a ureter. Stones under 5 mm in diameter (less than one-fifth of an inch) are often eliminated on their own (Fallon 2015; UMMC 2013).

The hallmark symptom of a kidney stone lodged in or obstructing a ureter is severe flank pain that comes on suddenly and is distinctly one-sided. The pain may wax and wane, but typically does not go away. Nausea and vomiting frequently accompany the pain, which can radiate to the front of the body or the groin, depending on where the stone is lodged (Curhan 2012). A stone that moves closer to the bladder may cause a frequent urge to urinate or a burning sensation with urination (UMMC 2013). Blood may be visible in the urine, and in some cases this is the only symptom (Curhan 2012). Fever may indicate the presence of a urinary tract infection in addition to stones (UMMC 2013).

6 Diagnosis

Many people with kidney stones do not have any symptoms. For this reason, kidney stones are sometimes found during a diagnostic imaging exam such as an abdominal X-ray, CT scan, or ultrasound that is being performed for another reason (Antonelli 2015).

Chronic and Recurrent Kidney Stones

After a stone is passed or surgically removed, it is typically analyzed for composition (Antonelli 2015; Curhan 2012). Diagnosis and prevention often relies on the 24-hour urine analysis, a valuable test that evaluates concentrations of calcium, magnesium, potassium, oxalate, citrate, and uric acid, as well as urine pH (LabCorp 2015). Obtaining two separate 24-hour urine analyses is a superior method of evaluation compared to a single test (Xu 2013; Sakhaee, Maalouf 2012; Healy 2012; Curhan 2012; Coe 2015).

Acute Kidney Stones

During acute kidney stone passage, blood tests are usually normal, though an elevated number of white blood cells may be seen (Curhan 2012; UMMC 2013). Red and white blood cells, as well as microscopic crystals, may be detected by urinalysis (Curhan 2012). Conditions that can cause symptoms similar to acute kidney stones include urinary tract infection, kidney infection, diverticulitis, ovarian diseases, appendicitis, and ectopic pregnancy (Aliotta 2015).

 A patient’s history, physical exam, and urinalysis often clearly indicate acute kidney stones, and diagnostic imaging may not be necessary to confirm the diagnosis in some cases (UMMC 2013; Curhan 2012). Helical computed tomography (CT) is typically used when diagnostic imaging is necessary (Curhan 2012). Ultrasound is not as sensitive as non-contrast CT but is preferred to limit radiation exposure in children and pregnant women (UMMC 2013; Aliotta 2015; Curhan 2012).

7 Conventional Treatment

The treatment approach to kidney stones depends on a number of factors and circumstances. For example, asymptomatic stones discovered during diagnostic imaging may not be treated, but an acute symptomatic kidney stone demands an intervention, even if only hydration and painkillers for a small stone (Curhan 2012; UMMC 2013). The high recurrence rate makes long-term prevention a priority for people with a history of kidney stones (Xu 2013).

The most important aspect of treatment and prevention is identifying the type of stone the patient has. A 24-hour urinalysis with saturation can be used to evaluate the tendency of a patient’s urine to form stones. Passed stones can be directly analyzed as well. Unfortunately, the reliability of kidney stone crystal analysis is not perfect; so if you received a diagnosis of a particular stone type, but preventive treatment has failed, it may be worthwhile to ask your doctor about conducting a reanalysis of your stone(s) (UCKSETP 2015; Krambeck 2010; LabCorp 2015).

Asymptomatic Stones

Stones that do not cause symptoms may be found incidentally during an imaging test (Bansal 2009). Asymptomatic stones under 6 mm are generally left untreated. The approach to larger stones, however, may vary: some practitioners will opt for preventive lithotripsy while others will adopt a wait-and-see approach (Curhan 2012). Other factors may influence the decision to treat asymptomatic kidney stones. For instance, airline pilots are not allowed to fly with asymptomatic kidney stones, due to the possibility of grave consequences of their being incapacitated while on duty (Portis 2001).

Acute Stones

Once a diagnosis of acute kidney stones is made, the top treatment priority is usually oral or intravenous pain management. Intravenous hydration may be used, and antibiotics may be necessary when infection is present (Curhan 2012; Frassetto 2011). Infection complicated by obstruction is a medical emergency that requires placement of a drainage device (Curhan 2012).

Medications that relax the ureters and prevent ureteral spasm may be used to promote the passage of stones, a practice called medical expulsive therapy. This approach may include the use of calcium channel blockers like nifedipine (Procardia) and alpha-blockers like tamsulosin (Flomax) for four to six weeks (Antonelli 2015).

Stones larger than 10 mm or that do not respond to conservative treatment may be treated with lithotripsy, ureteroscopy, or rarely, open surgery (Antonelli 2015).

Lithotripsy. Lithotripsy is the least invasive technique for treating kidney stones. In lithotripsy, shock waves are transmitted into the body, focused on the stone. This causes the stone to break into smaller fragments that can then pass more easily. This technique is also called extracorporeal shock wave lithotripsy (Antonelli 2015).

Ureteroscopy. In ureteroscopy a scope is passed through the urethra and bladder and into the ureter. When the scope reaches the stone, the stone can be fragmented with a laser or grasped with a basket and removed (Antonelli 2015).

Nephrolithotomy and nephrolithotripsy. These procedures involve the use of a minimally invasive surgical technique: a small incision is made to access the kidney or upper ureter with a nephroscope, which is then used to fragment (nephrolithotripsy) or remove (nephrolithotomy) the stone (Vicentini 2009; Antonelli 2015).

Laparoscopic and open surgeries. With advances over the past two decades in lithotripsy and other minimally invasive techniques, open surgery is performed far less frequently. These surgical techniques for direct stone removal are reserved for cases, usually with larger stones, when other methods are not appropriate (Antonelli 2015).

Medical Preventive Treatments 

About half of all people who have had one episode of kidney stones will have another episode within seven years if no treatment is undertaken (Xu 2013). Preventive strategies depend to a large degree on the type of stone, but for all stones, proper hydration is of the utmost importance (Morton 2002; Sakhaee, Maalouf 2012).

In some cases, preventive treatment entails addressing an underlying condition that predisposes to stone formation. For instance, 10% of calcium-containing stones are caused by medical conditions, including hyperparathyroidism. However, conventional medicine considers the majority of cases idiopathic, meaning the cause is unknown (Marangella 2008; Aliotta 2015; Curhan 2012).

Allopurinol. Allopurinol (Zyloprim) inhibits uric acid production in the body and is used as a treatment for both calcium oxalate and uric acid stones when uric acid is elevated (Sarig 1987; Arrabal-Polo, Arrabal-Martin 2013). Possible side effects of allopurinol include rash, digestive upset, and elevated liver enzymes (Xu 2013).

Thiazide diuretics. Thiazide diuretic medications are typically used to treat high blood pressure, but they also decrease urinary calcium. They have been found to be effective for preventing recurrence of calcium oxalate and calcium phosphate stones in people with high as well as normal urine calcium concentrations (Arrabal-Polo, Arrabal-Martin 2013; Xu 2013). Examples of thiazide diuretics are hydrochlorothiazide (Microzide), chlorthalidone (Thalitone, Hygroton), and indapamide (Lozol).

The usefulness of thiazide diuretics is limited by a number of negative side effects including low blood pressure; elevated blood glucose, uric acid, cholesterol, and triglyceride levels; and magnesium, citrate, and potassium loss (Heseltine 1988; Rohlfing 1986; Xu 2013). It has been suggested that thiazides may work better if used in combination with potassium citrate therapy and a low-salt diet (Sakhaee, Maalouf 2012).

Cystinuria treatment. Medications that split cystine into two molecules are used to prevent cystine stones in people with cystinuria. Such medications include d-penicillamine (Cuprimine) and alpha-mercaptopropionylglycine. Penicillamine can have severe side effects that include bone marrow suppression, blood disorders, kidney disease, and kidney failure (NLM 2012; Sakhaee, Maalouf 2012). Captopril (Capoten) has also been used for cystine stones, and has a more favorable side effect profile (Sloand 1987; Aliotta 2015).

8 Novel and Emerging Strategies


Hypercalciuria (high urine calcium concentration) is associated with both calcium kidney stones and bone loss (Xu 2013; Arrabal-Polo, Sierra Giron-Prieto 2013). Some researchers are beginning to explore the effect of a class of osteoporosis medications called bisphosphonates, such as alendronate (Fosamax), risedronate (Actonel), and ibandronate (Boniva), on calcium kidney stone risk (Grover 2013). These medications help keep urine calcium concentrations from rising by reducing bone breakdown and calcium loss (Bianchi 2010).

In one trial, 16 people placed on experimental bed rest for 3 weeks (in order to increase urinary calcium excretion by causing bone breakdown) and treated with 20 mg per day of the bisphosphonate alendronate had lower urine calcium concentrations, and lower calcium oxalate and calcium phosphate saturations, compared with placebo (Ruml 1995). In another trial, 70 individuals with recurrent calcium kidney stones, high urine calcium concentration, and bone loss were treated with either 70 mg per week of alendronate or 70 mg per week of alendronate plus 50 mg per day of the diuretic hydrochlorothiazide. After two years of treatment, an increase in bone mineral density and a decrease in urine calcium concentration was seen with both medication regimens, but the group treated with alendronate plus hydrochlorothiazide had more improvement than the group treated with alendronate alone (Arrabal-Polo, Arias-Santiago 2013).

While these findings are intriguing, they do not clearly establish whether alendronate or other bisphosphonates can prevent calcium kidney stone formation; in addition, some questions remain about the long-term safety of bisphosphonate use (Suresh 2014).

Sleep Position

Many people with recurrent kidney stones get them only on one side, leading some researchers to examine whether sleep position can predict the side on which stones occur. In a study of 110 unilateral (one-sided) kidney stone formers, 93 were found to sleep predominantly on one side, and of these, 71 (76%) slept on the same side as that of their stones (Shekarriz 2001). In a study in unilateral stone formers, 88% of participants with right-sided kidney stones slept right side down, and 62% of participants with left-sided stones slept left side down (Ziaee 2008).

Oxalobacter formigenes (Probiotic)

Oxalobacter formigenes (O. formigenes) is a bacterium found in the human digestive tract. It digests and metabolizes oxalate, preventing high urine oxalate and calcium oxalate kidney stones (Mogna 2014; Knight 2013). Several studies have found that antibiotic use can lead to the loss of O. formigenes colonies (Knight 2013).

One study found that patients with greater O. formigenes colonization had significantly lower urine oxalate levels (Kwak 2003). Stool cultures from recurrent calcium oxalate stone formers show that they are only about half as likely to have colonies of this bacterium compared with non-stone formers, and those with O. formigenes colonies have as much as 70% lower odds of calcium oxalate stone recurrence (Knight 2013; Kaufman 2008).

In a rodent model of severe hyperoxaluria, administration of O. formigenes as a probiotic supplement reduced urinary oxalate in just two days (Sidhu 2001). In a randomized controlled trial in 42 patients with the rare genetic condition primary hyperoxaluria, oral supplementation with O. formigenes resulted in more than twice the reduction of oxalate relative to urine creatinine compared to placebo. In those with the highest baseline oxalate concentrations, the reduction of urine oxalate was more than four times that of placebo (Hoppe 2011).

O. formigenes has been developed into a biopharmaceutical preparation and is not available as a dietary supplement at this time.

9 Dietary and Lifestyle Considerations

Increase Fluid Intake

Fluid intake is ordinarily the most influential factor in determining urine volume and thus kidney stone risk (Curhan 2012), and drinking adequate volumes of fluids may be the most effective intervention for people with any type of kidney stone (UMMC 2013). Most individuals who have had a kidney stone should drink at least 2 L of water per day (Arrabal-Polo, Arrabal-Martin 2013; Aliotta 2015). In a study in 199 people monitored for five years following a kidney stone episode, subjects who increased their fluid intake enough to maintain a urine volume of 2 L or more per day had less than half the risk of recurrence compared with those who did not (Borghi 1996).

Citrus juices. Lemon and orange juice are good sources of citrate, help alkalinize the urine, and appear to protect against kidney stones (UMMC 2013; Kang 2007; Haleblian 2008; Trinchieri 2002; Ferraro 2013).

Drinking lemon juice increases the amount of citrate in urine and may prevent kidney stones (UMMC 2013). A preliminary study found that daily consumption of a mixture of 2 L of water, 4 ounces of reconstituted lemon juice, and an artificial sweetener increased urine citrate concentrations and reduced stone formation in people with hypocitraturia-related kidney stones (Kang 2007).

Orange juice appears to be protective as well: in an analysis of three large studies, people who drank the most orange juice were found to be 12% less likely to develop kidney stones than those who drank the least (Ferraro 2013).

Mineral water. Mineral water combines several properties with known efficacy for preventing kidney stone disease and stone recurrence. Water dilutes urine, the minerals calcium and magnesium help bind dietary oxalate and reduce calcium oxalate crystallization, and the carbonate in mineral water alkalinizes urine and provides substrate for citrate formation (Siener 2004; Rodgers 1997; Rodgers 1998; Trinchieri 1999; Karagulle 2007).

Although several studies have demonstrated a benefit of mineral water for stone formers, further controlled studies that more clearly establish this benefit, especially compared to tap water or other beverages, are needed.

Eat More Fruits and Vegetables

Fruits and vegetables exert protective effects against most types of kidney stones. They generally have a high water content, which increases urine volume, have an alkalizing effect on urine, increase urinary citrate, and are naturally low in sodium and rich in potassium and magnesium. Fruits and vegetables are also high in compounds called phytates, which inhibit calcium crystal formation in the urine and are associated with a lower stone risk (Sorensen 2014; Curhan 2004; Borghi 2006).

In a study in almost 84 000 postmenopausal women, intake of fiber, fruits, and vegetables were each associated with lower risk of first-time kidney stone episodes. Comparing women with the highest to those with the lowest intakes, fiber was associated with up to a 26% risk reduction, fruits up to a 25% reduction, and vegetables up to a 22% reduction (Sorensen 2014).

Reduce Sodium Intake

Sodium increases the amount of calcium in the urine (Friedlander 2015), and high sodium intake has been correlated with increased kidney stone risk (Sorensen, Kahn 2012). In one trial, individuals with calcium kidney stone disease and high urine calcium concentrations were instructed to increase their fluid intake to 2–3 L per day. They were then randomly assigned to either a low-sodium diet group or a normal diet. After three months, those on the restricted sodium diet had lower urine calcium and oxalate concentrations than people in the normal diet group (Nouvenne 2010). Sodium restriction may also be useful for preventing recurrence of cystine stones, since lower amounts of sodium in the urine are associated with lower urine cystine concentrations (Heilberg 2013).

Reduce Sugar Intake

Several studies suggest higher consumption of refined sugar, particularly fructose and sugar-sweetened sodas, increases urine and serum uric acid levels and kidney stone risk (Ferraro 2013; Bantle 2009; Curhan 2004; Friedlander 2015; Taylor 2008).

The effects of soda and other beverages on kidney stone risk were evaluated in an analysis of three large studies that together included over 194 000 people. The authors found that drinking sugar-sweetened beverages increased stone risk: drinking one or more sugary colas per day was associated with a 23% higher risk of kidney stones compared to drinking less than one per week, while daily consumption of non-cola sugar-sweetened drinks was associated with a 33% higher risk (Ferraro 2013).

Consume Adequate Dietary Calcium

It used to be believed that calcium from diet and supplements increased kidney stone risk, and conventional physicians even advised kidney stone patients to reduce calcium consumption. However, a rigorous review of 10 studies found calcium supplementation does not increase stone risk (Candelas 2012), and low calcium intake has now been linked to increased kidney stone risk (Martini 2002). For a more detailed discussion of calcium and kidney stones, see the “Integrative Interventions” section.

Reduce Dietary Purine Intake

Purines (nitrogenous organic compounds that form part of the chemical structure of DNA) can be metabolized into uric acid, which can increase the risk of uric acid and calcium oxalate stones. Uric acid comes from the breakdown of purines which are made in the body by normal metabolic processes, or may be present in the diet (Boza 2000; Yamaoka 1996; Ishikawa 2013). Foods highest in purines are organ meats and seafood, legumes, and brewers and baker’s yeast (UMMC 2013; PAMF 2010; Mayo Clinic 2015a). Eating a high-purine diet can increase both urine and blood uric acid levels (Kenny 2010). People with kidney stones related to high uric acid levels are typically advised to avoid purine-rich foods (UMMC 2013), but a low-animal protein or vegetarian diet that alkalinizes the urine is more important for preventing uric acid stone formation (Kenny 2010; Heilberg 2013; Kanbara 2010).

Reduce Dietary Oxalate Intake

While high urine oxalate concentrations increase risk of calcium oxalate stones, and a low-oxalate diet has traditionally been recommended for preventing recurrence of calcium oxalate kidney stones. Oxalate is present in many foods, and combines with calcium to for calcium oxalate stones (Xu 2013; Friedlander 2015; Assimos 2004).

Digestive diseases, including inflammatory bowel diseases, and bariatric weight loss surgery can result in increased absorption of oxalate from food, so stone formers with these histories may benefit from avoiding high-oxalate foods (Xu 2013; Nazzal 2015). Beets, okra, spinach, Swiss chard, French fries, sweet potatoes, nuts, tea, chocolate, and soy products are examples of oxalate-rich foods that may be eliminated or restricted on a low-oxalate diet (Mayo Clinic 2015b; Cleveland Clinic 2015). Adequate calcium intake may ameliorates risk of calcium oxalate stone formation by binding oxalate in the gut and preventing its absorption (Trinchieri 2013; Sorensen, Kahn 2012; Nazzal 2015).

The DASH Diet and Kidney Stones

The Dietary Approaches to Stop Hypertension (DASH) diet emphasizes fruits and vegetables, nuts, legumes, whole grains, and low-fat dairy products, and limits saturated fat, sodium, total fat, cholesterol, refined grains, sweets, and red and processed meats (Taylor 2009; Noori 2014).

In an analysis of the nutrition data of more than 241 000 participants from three large population studies, each individual’s diet was graded for adherence to a low-sodium DASH-style diet. People with the highest scores, reflecting the closest adherence to DASH guidelines, were 40–45% less likely to develop kidney stones than people with the lowest scores (Taylor 2009).

In another study, 57 subjects with recurrent kidney stones and high urinary oxalate were randomly assigned to a low-sodium DASH diet or a low-oxalate diet group. Both diets were associated with improvements in urine chemistry with respect to kidney stone risk, but people on the DASH diet had higher urine pH (more alkaline urine) and greater urine citrate concentrations than those on the low-oxalate diet (Noori 2014). The DASH diet’s high citrate and calcium content may account for lower kidney stone risk among those adhering to this dietary approach (Taylor 2009).

10 Nutrients


Magnesium favorably impacts calcium oxalate stone-forming risk through multiple mechanisms. Magnesium binds oxalate in the digestive tract and inhibits the formation of calcium oxalate crystals in urine (Kohri 1988; Massey 2005). And higher magnesium consumption is significantly associated with lower risk of kidney stones (Negri 2013; Zimmermann 2005).

A study in over 45 000 US male health professionals found that those in the highest one-fifth of magnesium intake had a 29% lower risk of developing kidney stones (Taylor 2004). Another study in 311 patients with kidney stone disease evaluated magnesium levels in urine, a known marker of dietary intake of magnesium. In this population, higher urine magnesium was significantly correlated with lower urine oxalate (Eisner 2012).

The timing of magnesium supplement consumption may be important in the context of kidney stones. Magnesium must be present in the digestive tract at the same time as oxalate-containing foods in order to bind dietary oxalate and prevent it from being absorbed into general circulation, where the oxalate then has to be filtered by the kidneys, and is excreted into the urine. In a clinical study of six healthy volunteers, researchers noted administration of a magnesium supplement together with oxalate decreased oxalate absorption, whereas consumption of magnesium supplements 12 hours apart from oxalate administration did not have this effect (Zimmermann 2005).


A low-calcium diet is associated with a higher risk for calcium oxalate stones (Xu 2013). High dietary calcium, on the other hand, even when accompanied by a large increase in oxalate consumption, has been demonstrated to decrease kidney stone risk rather than increase it (Hess 1998; Sorensen, Kahn 2012; Taylor 2004). This is thought to be due to calcium’s ability to bind dietary oxalate in the intestines, which prevents oxalate absorption into the bloodstream, and eventually the kidneys and urine (Nazzal 2015). Consuming adequate calcium through diet and supplementation is associated with higher bone-mineral density (Napoli 2007). This may be another way adequate calcium intake helps prevent kidney stones. As bone mineral density decreases, urinary calcium content and stone risk increase (Arrabal-Polo, Sierra Giron-Prieto 2013). Bone resorption, or the breakdown of bone, causes calcium to leach into the blood and eventually the urine, increasing stone risk. Adequate calcium intake reduces bone resorption, conferring protection against kidney stones (Ettinger 2014; Heaney 2008; Martini 2002). 

In a study in over 45 000 male health professionals without kidney stones who were followed for up to 14 years, men under the age of 60 who were in the highest one-fifth of dietary calcium consumption had a 31% lower risk of kidney stones compared with the one-fifth who consumed the least calcium (Taylor 2004). Another study in over 78 000 women without kidney stone disease found that higher dietary calcium was associated with a 5‒28% reduction in kidney stone risk, and a study in over 96 000 younger women without kidney stones found that those in the highest one-fifth of dietary calcium consumption had a 27% lower risk of kidney stones compared with those in the lowest one-fifth (Sorensen, Kahn 2012; Curhan 2004).

Calcium supplements improve urine chemistry parameters and lower kidney stone risk, even in those on a low-oxalate diet. A study in 32 healthy young men with no history of kidney stones found that calcium supplementation, combined with a low-oxalate diet, lowered urine oxalate (Stitchantrakul 2004).

It has been suggested that calcium supplements should be taken with meals in order to bind the maximal amount of dietary oxalate (Domrongkitchaiporn 2004; Heilberg 2013).

Mineral Citrates

The most common types of kidney stones, calcium oxalate and uric acid, tend to form in acidic urine. Formation of the most uncommon kidney stones, cystine stones, also occurs in acidic urine (Frassetto 2011). Citrate protects against these types of stones by alkalinizing urine, binding calcium in the gut and in the urine, and inhibiting calcium oxalate crystallization (Goldberg 1989; Nicar 1987; Krieger 2015; Berg 1992). It is not surprising, then, that low urine citrate is a common finding in patients with these types of stones (Caudarella 2009). Mineral citrates, including calcium, magnesium, and potassium, are used in clinical practice and in research to increase urinary citrate, alkalinize urine, and reduce the rate of stone formation (Caudarella 2009; del Valle 2013; Sakhaee 2004; Ettinger 1997).

Magnesium, potassium, and calcium citrate. Both magnesium and citrate inhibit calcium oxalate crystal formation, though the combination of the two may be more effective than either alone (Rodgers 1999).

In a randomized controlled trial in 64 people with a history of calcium oxalate kidney stones, three years of potassium-magnesium citrate supplementation providing about 255 mg of magnesium resulted in an 85% reduction in kidney stone risk compared with placebo (Ettinger 1997). In a double-blind placebo-controlled trial in 20 participants who were put on bed rest for five weeks (in order to increase urinary calcium excretion), potassium-magnesium citrate supplementation effectively alkalinized the urine, increased citrate concentration and reduced uric acid concentration in the urine, and reduced calcium oxalate crystallization potential (Zerwekh 2007).  

Studies that used several different mineral preparations of potassium and magnesium found that adding a magnesium supplement to potassium citrate therapy, or using potassium-magnesium citrate, yielded superior results for improving urine chemistry compared to treatment without magnesium (Jaipakdee 2004; Kato 2004).

Potassium citrate is used in medicine to alkalinize urine, increase urine citrate, inhibit aggregation of calcium oxalate and calcium phosphate crystals, and reduce the risk of kidney stones (Arrabal-Polo, Arrabal-Martin 2013; Xu 2013; Sakhaee, Griffith 2012).

The dosage of potassium citrate used to prevent kidney stones is generally 1200–2400 mg per day, a prescription-strength dose that frequently causes digestive upset, making it intolerable for some people (Xu 2013). Potassium citrate dietary supplements usually do not contain more than 99 mg of potassium per pill. Potassium citrate is a less concentrated source of urine-alkalinizing citrate than the magnesium or calcium forms of citrate (Higdon 2010).

A study that used a supplement containing calcium citrate and potassium citrate improved urine chemistry by reducing acidity and increasing urinary citrate in people who had undergone gastric bypass surgery. The investigators concluded that potassium-calcium citrate might be helpful for decreasing kidney stone risk in this population (Sakhaee, Griffith 2012).


The bacterial population of the gastrointestinal tract may play an important role in oxalate breakdown and metabolism, and thus in the prevention of kidney stones (Miller 2013; Murphy 2009).

Several genera of probiotic bacteria, including Lactobacillus and Bifidobacteria, appear to be capable of metabolizing oxalate, thus reducing urinary oxalate and decreasing kidney stone risk. In an uncontrolled trial, six people with calcium oxalate kidney stone disease and high urinary oxalate concentrations consumed a supplement containing Lactobacillus and Bifidobacterium strains for four weeks. Urinary oxalate concentrations dropped by nearly half at the end of the study (Campieri 2001). In a subsequent trial of 10 patients with excessive intestinal oxalate absorption (caused by several different medical conditions), the patients were administered a probiotic formula that contained Lactobacillus and Bifidobacterium strains. Average urine oxalate fell by 19% after one month on a dosage of 8.5 billion bacteria daily; during the second month, oxalate excretion was reduced by 24% at a dosage of two per day (Lieske 2005). However, later trials using the same probiotic formulation were unable to demonstrate the same beneficial effect (Lieske 2010; Goldfarb 2007).

Another preliminary trial examined the effect of a probiotic supplement containing several Bifidobacterium and Lactobacillus strainsin 11 healthy people. Oxalate absorption was reduced after four weeks of probiotic supplementation, an effect largely attributable to the marked reduction observed in individuals who were high oxalate absorbers at the beginning of the study (Okombo 2010). Another study in 14 stone-forming individuals without hyperoxaluria administered a probiotic supplementthree times per day after meals, for two weeks, along with a high-oxalate diet. Half the study subjects experienced a reduction in urinary oxalate; the greatest reduction was in the two individuals who had the greatest increase in urinary oxalate during the high-oxalate diet (Ferraz 2009). A laboratory study of different bacterial strains found that Lactobacillus species exhibited greater oxalate-degrading ability compared with Bifidobacteria (Mogna 2014). 

Vitamin B6

Vitamin B6 deficiency affects as much as 24% of US adults, and may in part be induced by a high-protein diet. Inadequate vitamin B6 increases urine oxalate and kidney stone risk in laboratory animals and humans, and hyperoxaluria has been successfully reduced with vitamin B6 supplementation (Murthy 1982; Nath 1990; Kim 2014; Mitwalli 1988; Massey 2003). In a 14-year study in 85 557 women, kidney stone risk was 34% lower in women who consumed the most vitamin B6 per day from diet and supplements compared with those who consumed the least (Curhan 1999). In one study, 149 people with recurrent kidney stones were treated with 100 mg three times daily of magnesium oxide plus 10 mg once daily of vitamin B6 for 4.5‒6 years. The recurrence rate fell from an average of 1.3 per year to 0.1 per year during treatment, a 92% reduction (Prien 1974).  

Fish Oil

Some studies have found that supplementation with the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from fish oil may reduce kidney stone risk by lowering urine calcium. In one study, people with a history of kidney stones were treated with a short course (three months) and long course (18 months) of 1800 mg EPA daily. Urine calcium concentrations dropped in people who entered the study with high urinary calcium, but not in those with normal urinary calcium (Yasui 2001). In another study, 15 healthy people were given 900 mg EPA and 600 mg DHA daily for 30 days; excessive urinary oxalate excretion and calcium oxalate saturation was decreased at the end of the trial (Siener 2011). These studies suggest a possible role for fish oil in calcium oxalate kidney stone prevention.


N-acetylcysteine (NAC) is used by cells to replenish glutathione and detoxify free radicals (Zhang 2011; Rushworth 2014). A study with separate laboratory, preclinical, and clinical components found all three lines of evidence indicated potential for NAC to prevent the formation of calcium oxalate crystals and kidney stones. In the clinical phase of this trial, 17 people with calcium oxalate kidney stones were treated with 3 g per day of NAC. After one week of treatment, the number of large urinary calcium oxalate crystals was reduced by 60%, and three people experienced spontaneous passage of stones (Fan 1994). Findings from laboratory and animal studies provide additional evidence that NAC may reduce calcium oxalate crystallization and protect kidney cells from the damaging effects of calcium oxalate (Bijarnia 2008; Fishman 2013; Davalos 2010). NAC has also demonstrated activity that may help improve insulin sensitivity and protect against type 2 diabetes through multiple mechanisms (Lasram 2015). Since insulin resistance appears to be associated with kidney stone risk (Assimos 2004; Wong 2015), NAC holds promise as an integrative strategy for kidney stone prevention. 

Vitamin E

Vitamin E protects lipid molecules in cells and in the blood from oxidative damage and stress (Princen 1995; Ni 2012). In a laboratory study, vitamin E protected animal kidney cells from oxidative damage due to high oxalate conditions, suggesting it may play a role in preventing crystal deposition and stone initiation. The protective effect of vitamin E seen in this study was enhanced by the addition of the antioxidant vitamin C (Thamilselvan 2014). Animal studies have found that vitamin E inhibits stone initiation by reducing calcium oxalate crystallization, inhibiting crystal deposition in kidney tubule cells, and protecting against oxidative injury in kidney cells (Huang 2006; Thamilselvan 2005).

Green Tea and Catechins

Green tea and green tea extracts, which are rich in phytochemicals called catechins, have been shown to inhibit calcium oxalate stone formation (Jeong 2006; Itoh 2005; Graham 1992). In an animal study, the flavonoids catechin and epicatechin were evaluated for their ability to modulate kidney stone biochemical risk factors. Compared with rats given no treatment, those that received catechin or epicatechin had lower kidney calcium and fewer crystals deposited in the kidneys. The authors of the study suggested the flavonoids may have protected the interior of the kidneys from oxidative damage that could initiate stone formation (Grases 2009).

Another study, with laboratory and rodent model components, investigated the effects of catechin on calcium oxalate-mediated kidney damage. In the laboratory setting, catechin protected kidney cells from the oxidative stress ordinarily induced by calcium oxalate. In the animal component of the study, catechin appeared to protect rats from the oxidative effects of calcium oxalate (Zhai 2013).


The flavonoid quercetin has been studied in laboratory and preclinical models for its protective effect on kidney stone formation. One animal trial compared a mixture of quercetin and the related molecule hyperoside to potassium citrate for treating oxalate stones. The quercetin-hyperoside mixture decreased the amount of crystal deposits in kidney tissue compared with potassium citrate, and antioxidant enzyme activity was increased (Zhu 2014). In another study with both animal and lab components, quercetin protected against oxalate-induced damage in both settings, and protected against calcium oxalate crystal formation in rat kidneys (Park 2008).

Disclaimer and Safety Information

This information (and any accompanying material) is not intended to replace the attention or advice of a physician or other qualified health care professional. Anyone who wishes to embark on any dietary, drug, exercise, or other lifestyle change intended to prevent or treat a specific disease or condition should first consult with and seek clearance from a physician or other qualified health care professional. Pregnant women in particular should seek the advice of a physician before using any protocol listed on this website. The protocols described on this website are for adults only, unless otherwise specified. Product labels may contain important safety information and the most recent product information provided by the product manufacturers should be carefully reviewed prior to use to verify the dose, administration, and contraindications. National, state, and local laws may vary regarding the use and application of many of the therapies discussed. The reader assumes the risk of any injuries. The authors and publishers, their affiliates and assigns are not liable for any injury and/or damage to persons arising from this protocol and expressly disclaim responsibility for any adverse effects resulting from the use of the information contained herein.

The protocols raise many issues that are subject to change as new data emerge. None of our suggested protocol regimens can guarantee health benefits. Life Extension has not performed independent verification of the data contained in the referenced materials, and expressly disclaims responsibility for any error in the literature.

Adeva MM, Souto G. Diet-induced metabolic acidosis. Clinical nutrition (Edinburgh, Scotland). Aug 2011;30(4):416-421.

Aggarwal KP, Narula S, Kakkar M, Tandon C. Nephrolithiasis: molecular mechanism of renal stone formation and the critical role played by modulators. BioMed research international. 2013;2013:292953.

AHA. American Heart Association. Conditions: About Metabolic Syndrome. Available at Last updated 05/14/2014. Accessed 06/01/15.

Ahmadi F, Etemadi SM, Lessan-Pezeshki M, Mahdavi-Mazdeh M, Ayati M, Mir A, Yazdi HR. Contribution of stone size to chronic kidney disease in kidney stone formers. Int J Urol. Jan 2015;22(1):104-108.

Ahmed MH, Barakat S, Almobarak AO. The association between renal stone disease and cholesterol gallstones: the easy to believe and not hard to retrieve theory of the metabolic syndrome. Renal failure. Jul 2014;36(6):957-962.

Aliotta PJ, Alvero R. Ferri's Clinical Advisor. Urolithiasis (Nephrolithiasis). Available at: Copyright 2015. Accessed 4/10/2015.

Antonelli J, Maalouf N. ePocrates. Nephrolithiasis. Available at: Accessed 4/7/2015.

Arrabal-Polo MA, Arias-Santiago S, de Haro-Munoz T, Lopez-Ruiz A, Orgaz-Molina J, Gonzalez-Torres S, . . . Arrabal-Martin M. Effects of aminobisphosphonates and thiazides in patients with osteopenia/osteoporosis, hypercalciuria, and recurring renal calcium lithiasis. Urology. Apr 2013;81(4):731-737.

Arrabal-Polo MA, Arrabal-Martin M, Garrido-Gomez J. Calcium renal lithiasis: metabolic diagnosis and medical treatment. Sao Paulo medical journal = Revista paulista de medicina. 2013;131(1):46-53.

Arrabal-Polo MA, Sierra Giron-Prieto M, Orgaz-Molina J, Zuluaga-Gomez A, Arias-Santiago S, Arrabal-Martin M. Calcium renal lithiasis and bone mineral density. Importance of bone metabolism in urinary lithiasis. Actas Urol Esp. Jun 2013;37(6):362-367.

Assimos DG. Vitamin C supplementation and urinary oxalate excretion. Reviews in urology. Summer 2004;6(3):167.

Bansal AD, Hui J, Goldfarb DS. Asymptomatic nephrolithiasis detected by ultrasound. Clinical journal of the American Society of Nephrology: CJASN. Mar 2009;4(3):680-684.

Bantle JP. Dietary fructose and metabolic syndrome and diabetes. The Journal of nutrition. Jun 2009;139(6):1263S-1268S.

Baxmann AC, De OGMC, Heilberg IP. Effect of vitamin C supplements on urinary oxalate and pH in calcium stone-forming patients. Kidney international. 2003;63(3):1066-1071.

Berg C, Larsson L, Tiselius HG. The effects of a single evening dose of alkaline citrate on urine composition and calcium stone formation. J Urol. Sep 1992;148(3 Pt 2):979-985.

Bianchi G, Giusti A, Pioli G, Barone A, Palummeri E, Girasole G. Bisphosphonates in the management of idiopathic hypercalciuria associated with osteoporosis: a new trick from an old drug. Therapeutic advances in musculoskeletal disease. Feb 2010;2(1):29-35.

Bijarnia RK, Kaur T, Aggarwal K, Singla SK, Tandon C. Modulatory effects of N-acetylcysteine on hyperoxaluric manifestations in rat kidney. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. Jun 2008;46(6):2274-2278.

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. Mar 1996;155(3):839-843.

Borghi L, Meschi T, Maggiore U, Prati B. Dietary therapy in idiopathic nephrolithiasis. Nutrition reviews. Jul 2006;64(7 Pt 1):301-312.

Boza JJ, Moennoz D, Bournot CE, Blum S, Zbinden I, Finot PA, Ballevre O. Role of glutamine on the de novo purine nucleotide synthesis in Caco-2 cells. European journal of nutrition. Feb 2000;39(1):38-46.

Campieri C, Campieri M, Bertuzzi V, Swennen E, Matteuzzi D, Stefoni S, . . . De Simone C. Reduction of oxaluria after an oral course of lactic acid bacteria at high concentration. Kidney international. Sep 2001;60(3):1097-1105.

Candelas G, Martinez-Lopez JA, Rosario MP, Carmona L, Loza E. Calcium supplementation and kidney stone risk in osteoporosis: a systematic literature review. Clinical and experimental rheumatology. Nov-Dec 2012;30(6):954-961.

Caudarella R, Vescini F. Urinary citrate and renal stone disease: the preventive role of alkali citrate treatment. Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica / Associazione ricerche in urologia. Sep 2009;81(3):182-187.

Chines A, Boniface A, McAlister W, Whyte M. Hypercalciuria in osteogenesis imperfecta: a follow-up study to assess renal effects. Bone. Mar 1995;16(3):333-339.

Cleveland Clinic. Kidney Stones: Oxalate-Controlled Diet. Copyright 2015. Accessed 8/12/2015.

Coe F. The University of Chicago. Why 24 Hour Urine: Supersaturation. Accessed 7/31/2015.

Curhan G, Goldman L (ed.), SchaferAI  (ed.). Goldman's Cecil Medicine, Twenty-Fourth Edition. Chapter 128: Nephrolithiasis; 789-794. Copyright 2012 Saunders, an imprint of Elsevier, Inc. Available at: Accessed: 4/10/2015.

Curhan GC, Willett WC, Knight EL, Stampfer MJ. Dietary factors and the risk of incident kidney stones in younger women: Nurses' Health Study II. Archives of internal medicine. Apr 26 2004;164(8):885-891.

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. Apr 1 1997;126(7):497-504.

Curhan GC, Willett WC, Speizer FE, Stampfer MJ. Intake of vitamins B6 and C and the risk of kidney stones in women. Journal of the American Society of Nephrology : JASN. Apr 1999;10(4):840-845.

Davalos M, Konno S, Eshghi M, Choudhury M. Oxidative renal cell injury induced by calcium oxalate crystal and renoprotection with antioxidants: a possible role of oxidative stress in nephrolithiasis. Journal of endourology / Endourological Society. Mar 2010;24(3):339-345.

del Valle EE, Spivacow FR, Negri AL. [Citrate and renal stones]. Medicina (B Aires). 2013;73(4):363-368.

Domrongkitchaiporn S, Sopassathit W, Stitchantrakul W, Prapaipanich S, Ingsathit A, Rajatanavin R. Schedule of taking calcium supplement and the risk of nephrolithiasis. Kidney international. May 2004;65(5):1835-1841.

Eisner BH, Porten SP, Bechis SK, Stoller ML. Diabetic kidney stone formers excrete more oxalate and have lower urine pH than nondiabetic stone formers. J Urol. Jun 2010;183(6):2244-2248.

Eisner BH, Sheth S, Dretler SP, Herrick B, Pais VM, Jr. High dietary magnesium intake decreases hyperoxaluria in patients with nephrolithiasis. Urology. Oct 2012;80(4):780-783.

Escribano J, Balaguer A, Roque i Figuls M, Feliu A, Ferre N. Dietary interventions for preventing complications in idiopathic hypercalciuria. The Cochrane database of systematic reviews. 2014;2:CD006022.

Espinosa E, Murray T. Chapter 184: Kidney Stones (Renal Calculi, Nephrolithiasis). In: Textbook of Natural Medicine, 4th ed. Pizzorno JE, Murray MT (eds.). Copyright 2012 Churchill Livingstone, An Imprint of Elsevier.

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. Dec 1997;158(6):2069-2073.

Ettinger AS, Lamadrid-Figueroa H, Mercado-Garcia A, Kordas K, Wood RJ, Peterson KE, . . . Tellez-Rojo MM. Effect of calcium supplementation on bone resorption in pregnancy and the early postpartum: a randomized controlled trial in Mexican women. Nutrition journal. 2014;13(1):116.

Fallon B. University of Iowa Hospitals & Clinics. Health Library page. Kidney Stones. Copyright 2015. Accessed 7/31/2015.

Fan J, Shen SJ. The role of Tamm-Horsfall mucoprotein in calcium oxalate crystallization. N-acetylcysteine--a new therapy for calcium oxalate urolithiasis. Br J Urol. Sep 1994;74(3):288-293.

Fenton TR, Lyon AW. Milk and acid-base balance: proposed hypothesis versus scientific evidence. Journal of the American College of Nutrition. Oct 2011;30(5 Suppl 1):471s-475s.

Ferraro PM, Curhan GC, Gambaro G, Taylor EN. Total, Dietary, and Supplemental Vitamin C Intake and Risk of Incident Kidney Stones. American journal of kidney diseases : the official journal of the National Kidney Foundation. 2016;67(3):400-407.

Ferraro PM, Taylor EN, Gambaro G, Curhan GC. Soda and other beverages and the risk of kidney stones. Clinical journal of the American Society of Nephrology : CJASN. Aug 2013;8(8):1389-1395.

Ferraz RR, Marques NC, Froeder L, Menon VB, Siliano PR, Baxmann AC, Heilberg IP. Effects of Lactobacillus casei and Bifidobacterium breve on urinary oxalate excretion in nephrolithiasis patients. Urological research. Apr 2009;37(2):95-100.

Fishman AI, Green D, Lynch A, Choudhury M, Eshghi M, Konno S. Preventive effect of specific antioxidant on oxidative renal cell injury associated with renal crystal formation. Urology. Aug 2013;82(2):489 e481-487.

Frassetto L, Kohlstadt I. Treatment and prevention of kidney stones: an update. American family physician. Dec 1 2011;84(11):1234-1242.

Friedlander JI, Antonelli JA, Pearle MS. Diet: from food to stone. World J Urol. Feb 2015;33(2):179-185.

Garg A, Bonanome A, Grundy SM, Unger RH, Breslau NA, Pak CY. Effects of dietary carbohydrates on metabolism of calcium and other minerals in normal subjects and patients with noninsulin-dependent diabetes mellitus. The Journal of clinical endocrinology and metabolism. Apr 1990;70(4):1007-1013.

Gasser RW. Clinical aspects of primary hyperparathyroidism: clinical manifestations, diagnosis, and therapy. Wien Med Wochenschr. Sep 2013;163(17-18):397-402.

Gettman MT, Segura JW. Struvite stones: diagnosis and current treatment concepts. Journal of endourology / Endourological Society. Nov 1999;13(9):653-658.

Goldberg H, Grass L, Vogl R, Rapoport A, Oreopoulos DG. Urine citrate and renal stone disease. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. Aug 1 1989;141(3):217-221.

Goldfarb DS, Modersitzki F, Asplin JR. A randomized, controlled trial of lactic acid bacteria for idiopathic hyperoxaluria. Clinical journal of the American Society of Nephrology : CJASN. Jul 2007;2(4):745-749.

Graham HN. Green tea composition, consumption, and polyphenol chemistry. Preventive Medicine. 5// 1992;21(3):334-350.

Grases F, Prieto RM, Gomila I, Sanchis P, Costa-Bauza A. Phytotherapy and renal stones: the role of antioxidants. A pilot study in Wistar rats. Urological research. Feb 2009;37(1):35-40.

Grassi W, De Angelis R. Clinical features of gout. Reumatismo. 2011;63(4):238-245.

Grover A, LeBoff M. Osteoporosis: Prevention and Treatment. In: ENDOTEXT [Internet] De Groot LJ, Beck-Peccoz P, Chrousos G, et al, eds. South Dartmouth (MA):, Inc. Last updated 3/22/2013.

Gul Z, Monga M. Medical and dietary therapy for kidney stone prevention. Korean journal of urology. Dec 2014;55(12):775-779.

Halabe A, Sperling O. Uric acid nephrolithiasis. Mineral and electrolyte metabolism. 1994;20(6):424-431.

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. Journal of endourology / Endourological Society. Jun 2008;22(6):1359-1366.

Hartman C, Friedlander JI, Moreira DM, Elsamra SE, Smith AD, Okeke Z. Differences in 24-h urine composition between nephrolithiasis patients with and without diabetes mellitus. BJU Int. Apr 2015;115(4):619-624.

Healy KA, Hubosky SG, Bagley DH. 24-Hour Urine Collection in the Metabolic Evaluation of Stone Formers: Is One Study Adequate? Journal of Endourology. 2012;27(3):374-378.

Heaney RP. Calcium supplementation and incident kidney stone risk: a systematic review. Journal of the American College of Nutrition. Oct 2008;27(5):519-527.

Heilberg IP, Goldfarb DS. Optimum nutrition for kidney stone disease. Advances in chronic kidney disease. Mar 2013;20(2):165-174.

Heseltine D, Bramble MG. Loop diuretics cause less postural hypotension than thiazide diuretics in the frail elderly. Current medical research and opinion. 1988;11(4):232-235.

Hess B, Jost C, Zipperle L, Takkinen R, Jaeger P. High-calcium intake abolishes hyperoxaluria and reduces urinary crystallization during a 20-fold normal oxalate load in humans. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. Sep 1998;13(9):2241-2247.

Higdon J. Linus Pauling Institute. Micronutrient Information Center. Potassium. Last updated 12/2010. Accessed 8/6/2015.

Hoppe B, Groothoff JW, Hulton SA, Cochat P, Niaudet P, Kemper MJ, . . . Milliner D. Efficacy and safety of Oxalobacter formigenes to reduce urinary oxalate in primary hyperoxaluria. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. Nov 2011;26(11):3609-3615.

Huang HS, Chen J, Chen CF, Ma MC. Vitamin E attenuates crystal formation in rat kidneys: roles of renal tubular cell death and crystallization inhibitors. Kidney international. Aug 2006;70(4):699-710.

Husain A, Madhesia D. Heterocyclic compounds as carbonic anhydrase inhibitor. Journal of enzyme inhibition and medicinal chemistry. Dec 2012;27(6):773-783.

Ishikawa T, Aw W, Kaneko K. Metabolic Interactions of Purine Derivatives with Human ABC Transporter ABCG2: Genetic Testing to Assess Gout Risk. Pharmaceuticals (Basel, Switzerland). 2013;6(11):1347-1360.

Itoh Y, Yasui T, Okada A, Tozawa K, Hayashi Y, Kohri K. Preventive effects of green tea on renal stone formation and the role of oxidative stress in nephrolithiasis. J Urol. Jan 2005;173(1):271-275.

Jaipakdee S, Prasongwatana V, Premgamone A, Reungjui S, Tosukhowong P, Tungsanga K, . . . Sriboonlue P. The effects of potassium and magnesium supplementations on urinary risk factors of renal stone patients. Journal of the Medical Association of Thailand = Chotmaihet thangphaet. Mar 2004;87(3):255-263.

Jeong BC, Kim BS, Kim JI, Kim HH. Effects of green tea on urinary stone formation: an in vivo and in vitro study. Journal of endourology / Endourological Society. May 2006;20(5):356-361.

Johns Hopkins. Johns Hopkins Health Library. Kidney Stones.,P01494/. Accessed 7/17/2015.

Kanbara A, Hakoda M, Seyama I. Urine alkalization facilitates uric acid excretion. Nutrition journal. 2010;9:45.

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. Apr 2007;177(4):1358-1362; discussion 1362; quiz 1591.

Karagulle O, Smorag U, Candir F, Gundermann G, Jonas U, Becker AJ, . . . Gutenbrunner C. Clinical study on the effect of mineral waters containing bicarbonate on the risk of urinary stone formation in patients with multiple episodes of CaOx-urolithiasis. World J Urol. Jun 2007;25(3):315-323.

Kato Y, Yamaguchi S, Yachiku S, Nakazono S, Hori J, Wada N, Hou K. Changes in urinary parameters after oral administration of potassium-sodium citrate and magnesium oxide to prevent urolithiasis. Urology. Jan 2004;63(1):7-11; discussion 11-12.

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. Journal of the American Society of Nephrology : JASN. Jun 2008;19(6):1197-1203.

Kaur J. A comprehensive review on metabolic syndrome. Cardiology research and practice. 2014;2014:943162.

Keddis MT, Rule AD. Nephrolithiasis and loss of kidney function. Current opinion in nephrology and hypertension. Jul 2013;22(4):390-396.

Kenny JE, Goldfarb DS. Update on the pathophysiology and management of uric acid renal stones. Curr Rheumatol Rep. Apr 2010;12(2):125-129.

Kim YN, Cho YO. Evaluation of vitamin B6 intake and status of 20- to 64-year-old Koreans. Nutrition research and practice. Dec 2014;8(6):688-694.

Knight J, Deora R, Assimos DG, Holmes RP. The genetic composition of Oxalobacter formigenes and its relationship to colonization and calcium oxalate stone disease. Urolithiasis. Jun 2013;41(3):187-196.

Koeppen BM. The kidney and acid-base regulation. 2009;33(4):275-281.

Kohri K, Garside J, Blacklock NJ. The role of magnesium in calcium oxalate urolithiasis. Br J Urol. Feb 1988;61(2):107-115.

Krambeck AE, Khan NF, Jackson ME, Lingeman JE, McAteer JA, Williams JC, Jr. Inaccurate reporting of mineral composition by commercial stone analysis laboratories: implications for infection and metabolic stones. J Urol. Oct 2010;184(4):1543-1549.

Krieger NS, Asplin JR, Frick KK, Granja I, Culbertson CD, Ng A, . . . Bushinsky DA. Effect of Potassium Citrate on Calcium Phosphate Stones in a Model of Hypercalciuria. Journal of the American Society of Nephrology. April 8, 2015.

Kristensen C, Parks JH, Lindheimer M, Coe FL. Reduced glomerular filtration rate and hypercalciuria in primary struvite nephrolithiasis. Kidney international. Nov 1987;32(5):749-753.

Kwak C, Kim HK, Kim EC, Choi MS, Kim HH. Urinary oxalate levels and the enteric bacterium Oxalobacter formigenes in patients with calcium oxalate urolithiasis. European urology. Oct 2003;44(4):475-481.

LabCorp. LabCorp website: Test Menu: Kidney Stone Urine Test Combination With Saturation Calculations. Accessed 6/25/2015.

Lambert E, Arunachalam D. First Consult. Nephrolithiasis. Available at: Copyright Elsevier BV, Inc. Last updated 7/12/2012. Accessed 4/10/2015.

Lasram MM, Dhouib IB, El Fazaa S, Gharbi N. A review on the possible molecular mechanism of action of N-acetylcysteine against insulin resistance and type-2 diabetes development. Clin Biochem. Apr 25 2015.

Lewis JL. Merck Manual. Professional Version. Acid-Base Regulation. Last updated 2/2013. Accessed 7/31/2015.

Li H, Klett DE, Littleton R, Elder JS, Sammon JD. Role of insulin resistance in uric acid nephrolithiasis. World J Nephrol. Nov 6 2014;3(4):237-242.

Lieske JC, Goldfarb DS, De Simone C, Regnier C. Use of a probiotic to decrease enteric hyperoxaluria. Kidney international. Sep 2005;68(3):1244-1249.

Lieske JC, Tremaine WJ, De Simone C, O'Connor HM, Li X, Bergstralh EJ, Goldfarb DS. Diet, but not oral probiotics, effectively reduces urinary oxalate excretion and calcium oxalate supersaturation. Kidney international. Dec 2010;78(11):1178-1185.

Maalouf NM. Metabolic syndrome and the genesis of uric acid stones. Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation. Jan 2011;21(1):128-131.

Marangella M, Vitale C, Bagnis C, Petrarulo M, Tricerri A. Use of drugs for nephrolithiasis. Clin Cases Miner Bone Metab. May 2008;5(2):131-134.

Martini LA, Heilberg IP. Stop dietary calcium restriction in kidney stone-forming patients. Nutrition reviews. Jul 2002;60(7 Pt 1):212-214.

Massey LK. Dietary influences on urinary oxalate and risk of kidney stones. Front Biosci. May 1 2003;8:s584-594.

Massey L. Magnesium therapy for nephrolithiasis. Magnes Res. 2005;18(2):123-6.

Mayo Clinic. Patient Care & Health Info page. Nutrition and healthy eating. Gout diet: What's allowed, what's not. 4/11/2015a. Accessed 6/18/2015.

Mayo Clinic. Diseases and Conditions: Kidney Stones. Available at Last updated 02/26/2015b. Accessed 05/04/2015. 2015.

Miller AW, Dearing D. The metabolic and ecological interactions of oxalate-degrading bacteria in the Mammalian gut. Pathogens. 2013;2(4):636-652.

Mitwalli A, Ayiomamitis A, Grass L, Oreopoulos DG. Control of hyperoxaluria with large doses of pyridoxine in patients with kidney stones. International urology and nephrology. 1988;20(4):353-359.

Moe SM. Disorders involving calcium, phosphorus, and magnesium. Primary care. Jun 2008;35(2):215-237, v-vi.

Mogna L, Pane M, Nicola S, Raiteri E. Screening of different probiotic strains for their in vitro ability to metabolise oxalates: any prospective use in humans? Journal of clinical gastroenterology. Nov-Dec 2014;48 Suppl 1:S91-95.

Morris RC, Jr., Schmidlin O, Tanaka M, Forman A, Frassetto L, Sebastian A. Differing effects of supplemental KCl and KHCO3: pathophysiological and clinical implications. Seminars in nephrology. Sep 1999;19(5):487-493.

Morton AR, Iliescu EA, Wilson JW. Nephrology: 1. Investigation and treatment of recurrent kidney stones. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. Jan 22 2002;166(2):213-218.

Murphy C, Murphy S, O'Brien F, O'Donoghue M, Boileau T, Sunvold G, . . . O'Mahony L. Metabolic activity of probiotics-oxalate degradation. Vet Microbiol. Apr 14 2009;136(1-2):100-107.

Murthy MS, Farooqui S, Talwar HS, Thind SK, Nath R, Rajendran L, Bapna BC. Effect of pyridoxine supplementation on recurrent stone formers. Int J Clin Pharmacol Ther Toxicol. Sep 1982;20(9):434-437.

Napoli N, Thompson J, Civitelli R, Armamento-Villareal RC. Effects of dietary calcium compared with calcium supplements on estrogen metabolism and bone mineral density. The American journal of clinical nutrition. May 2007;85(5):1428-1433.

Nath R, Thind SK, Murthy MSR, Farooqui S, Gupta R, Koul HK. Role of Pyridoxine in Oxalate Metabolism. Annals of the New York Academy of Sciences. 1990;585(1):274-284.

Nazzal L, Puri S, Goldfarb DS. Enteric hyperoxaluria: an important cause of end-stage kidney disease. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. Feb 20 2015.

Negri AL, Spivacow FR, Del Valle EE. [Diet in the treatment of renal lithiasis. Pathophysiological basis]. Medicina (B Aires). 2013;73(3):267-271.

Ngo TC, Assimos DG. Uric Acid nephrolithiasis: recent progress and future directions. Reviews in urology. Winter 2007;9(1):17-27.

Ni Y, Eng C. Vitamin E protects against lipid peroxidation and rescues tumorigenic phenotypes in cowden/cowden-like patient-derived lymphoblast cells with germline SDHx variants. Clinical cancer research : an official journal of the American Association for Cancer Research. Sep 15 2012;18(18):4954-4961.

Nicar MJ, Hill K, Pak CY. Inhibition by citrate of spontaneous precipitation of calcium oxalate in vitro. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. Jun 1987;2(3):215-220.

NIDDK. National Institute of Diabetes and Digestive and Kidney Dseases. National Institutes of Health: Health nformaton: The Kidneys and How They Work. Available at Last updated 05/21/2014. Accessed 05/25/2015.

NIH. National Institutes of Health: National Institute of Diabetes and Digestive and Kidney Diseases: The Urinary Tract and How it Works. Available at Last updated 01/22/2014. Accessed 04/20/15.

NLM. National Library of Medicine. Kidney Stones (Renal Calculi). Accessed 7/17/2015.

NLM. US National Library of Medicine. Daily Med: Cuprimine. Available at Last updated 08/2012. Accessed 06/01/2015.

Noori N, Honarkar E, Goldfarb DS, Kalantar-Zadeh K, Taheri M, Shakhssalim N, . . . Basiri A. Urinary lithogenic risk profile in recurrent stone formers with hyperoxaluria: a randomized controlled trial comparing DASH (Dietary Approaches to Stop Hypertension)-style and low-oxalate diets. American journal of kidney diseases : the official journal of the National Kidney Foundation. Mar 2014;63(3):456-463.

Nouvenne A, Meschi T, Prati B, Guerra A, Allegri F, Vezzoli G, . . . Borghi L. Effects of a low-salt diet on idiopathic hypercalciuria in calcium-oxalate stone formers: a 3-mo randomized controlled trial. The American journal of clinical nutrition. Mar 2010;91(3):565-570.

Nussey S, Whitehead S. Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001.

Okombo J, Liebman M. Probiotic-induced reduction of gastrointestinal oxalate absorption in healthy subjects. Urological research. Jun 2010;38(3):169-178.

PAMF. Palo Alto Medical Foundation. Gout: Preventing Gout Attacks. Last updated 12/2010. Accessed 6/18/2015.

Pak CY, Sakhaee K, Fuller C. Successful management of uric acid nephrolithiasis with potassium citrate. Kidney international. Sep 1986;30(3):422-428.

Park HK, Jeong BC, Sung MK, Park MY, Choi EY, Kim BS, . . . Kim JI. Reduction of oxidative stress in cultured renal tubular cells and preventive effects on renal stone formation by the bioflavonoid quercetin. J Urol. Apr 2008;179(4):1620-1626.

Pena de la Vega L, Lieske JC, Milliner D, Gonyea J, Kelly DG. Urinary oxalate excretion increases in home parenteral nutrition patients on a higher intravenous ascorbic acid dose. JPEN. Journal of parenteral and enteral nutrition. Nov-Dec 2004;28(6):435-438.

Portis AJ, Sundaram CP. Diagnosis and initial management of kidney stones. American family physician. Apr 1 2001;63(7):1329-1338.

Preminger GM. Merck Manual. Professional Version. Urinary Calculi. Copyright 2015. Accessed 6/18/2015.

Prien EL, Sr., Gershoff SF. Magnesium oxide-pyridoxine therapy for recurrent calcium oxalate calculi. J Urol. Oct 1974;112(4):509-512.

Princen HM, van Duyvenvoorde W, Buytenhek R, van der Laarse A, van Poppel G, Gevers Leuven JA, van Hinsbergh VW. Supplementation with low doses of vitamin E protects LDL from lipid peroxidation in men and women. Arteriosclerosis, thrombosis, and vascular biology. Mar 1995;15(3):325-333.

Rodgers A. Aspects of calcium oxalate crystallization: theory, in vitro studies, and in vivo implementation. Journal of the American Society of Nephrology : JASN. Nov 1999;10 Suppl 14:S351-354.

Rodgers AL. Effect of mineral water containing calcium and magnesium on calcium oxalate urolithiasis risk factors. Urol Int. 1997;58(2):93-99.

Rodgers AL. The influence of South African mineral water on reduction of risk of calcium oxalate kidney stone formation. S Afr Med J. Apr 1998;88(4):448-451.

Rohlfing JJ, Brunzell JD. The effects of diuretics and adrenergic-blocking agents on plasma lipids. The Western journal of medicine. Aug 1986;145(2):210-218.

Ruml LA, Dubois SK, Roberts ML, Pak CY. Prevention of hypercalciuria and stone-forming propensity during prolonged bedrest by alendronate. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. Apr 1995;10(4):655-662.

Rushworth GF, Megson IL. Existing and potential therapeutic uses for N-acetylcysteine: the need for conversion to intracellular glutathione for antioxidant benefits. Pharmacology & therapeutics. Feb 2014;141(2):150-159.

Sakhaee K, Griffith C, Pak CY. Biochemical control of bone loss and stone-forming propensity by potassium-calcium citrate after bariatric surgery. Surg Obes Relat Dis. Jan-Feb 2012;8(1):67-72.

Sakhaee K, Maalouf NM. Metabolic syndrome and uric acid nephrolithiasis. Seminars in nephrology. Mar 2008;28(2):174-180.

Sakhaee K, Maalouf NM, Sinnott B. Clinical review. Kidney stones 2012: pathogenesis, diagnosis, and management. The Journal of clinical endocrinology and metabolism. Jun 2012;97(6):1847-1860.

Sakhaee K, Poindexter JR, Griffith CS, Pak CY. Stone forming risk of calcium citrate supplementation in healthy postmenopausal women. The Journal of urology. Sep 2004;172(3):958-961.

Sands JM, Layton HE. The physiology of urinary concentration: an update. Seminars in nephrology. May 2009;29(3):178-195.

Sarig S. The hyperuricosuric calcium oxalate stone former. Mineral and electrolyte metabolism. 1987;13(4):251-256.

Schwalfenberg GK. The Alkaline Diet: Is There Evidence That an Alkaline pH Diet Benefits Health? Journal of Environmental and Public Health. 2012;2012:727630.

Shekarriz B, Lu HF, Stoller ML. Correlation of unilateral urolithiasis with sleep posture. J Urol. Apr 2001;165(4):1085-1087.

Sidhu H, Allison MJ, Chow JM, Clark A, Peck AB. Rapid reversal of hyperoxaluria in a rat model after probiotic administration of Oxalobacter formigenes. J Urol. Oct 2001;166(4):1487-1491.

Siener R, Jahnen A, Hesse A. Influence of a mineral water rich in calcium, magnesium and bicarbonate on urine composition and the risk of calcium oxalate crystallization. European journal of clinical nutrition. Feb 2004;58(2):270-276.

Siener R, Jansen B, Watzer B, Hesse A. Effect of n-3 fatty acid supplementation on urinary risk factors for calcium oxalate stone formation. J Urol. Feb 2011;185(2):719-724.

Singh KJ, Kaur J. Comparison of three different endoscopic techniques in management of bladder calculi. Indian journal of urology : IJU : journal of the Urological Society of India. Jan 2011;27(1):10-13.

Sloand JA, Izzo JL, Jr. Captopril reduces urinary cystine excretion in cystinuria. Archives of internal medicine. Aug 1987;147(8):1409-1412.

Sorensen MD, Eisner BH, Stone KL, Kahn AJ, Lui LY, Sadetsky N, Stoller ML. Impact of calcium intake and intestinal calcium absorption on kidney stones in older women: the study of osteoporotic fractures. The Journal of urology. Apr 2012;187(4):1287-1292.

Sorensen MD, Hsi RS, Chi T, Shara N, Wactawski-Wende J, Kahn AJ, . . . Stoller ML. Dietary intake of fiber, fruit and vegetables decreases the risk of incident kidney stones in women: a Women's Health Initiative report. J Urol. Dec 2014;192(6):1694-1699.

Sorensen MD, Kahn AJ, Reiner AP, Tseng TY, Shikany JM, Wallace RB, . . . Stoller ML. Impact of nutritional factors on incident kidney stone formation: a report from the WHI OS. J Urol. May 2012;187(5):1645-1649.

Stitchantrakul W, Sopassathit W, Prapaipanich S, Domrongkitchaiporn S. Effects of calcium supplements on the risk of renal stone formation in a population with low oxalate intake. Southeast Asian J Trop Med Public Health. Dec 2004;35(4):1028-1033.

Suresh E, Pazianas M, Abrahamsen B. Safety issues with bisphosphonate therapy for osteoporosis. Rheumatology (Oxford, England). Jan 2014;53(1):19-31.

Taylor EN, Curhan GC. Fructose consumption and the risk of kidney stones. Kidney international. Jan 2008;73(2):207-212.

Taylor EN, Fung TT, Curhan GC. DASH-style diet associates with reduced risk for kidney stones. Journal of the American Society of Nephrology : JASN. Oct 2009;20(10):2253-2259.

Taylor EN, Stampfer MJ, Curhan GC. Dietary factors and the risk of incident kidney stones in men: new insights after 14 years of follow-up. Journal of the American Society of Nephrology : JASN. Dec 2004;15(12):3225-3232.

Thamilselvan S, Menon M. Vitamin E therapy prevents hyperoxaluria-induced calcium oxalate crystal deposition in the kidney by improving renal tissue antioxidant status. BJU Int. Jul 2005;96(1):117-126.

Thamilselvan V, Menon M, Thamilselvan S. Oxalate at physiological urine concentrations induces oxidative injury in renal epithelial cells: effect of alpha-tocopherol and ascorbic acid. BJU Int. Jul 2014;114(1):140-150.

Thom JA, Morris JE, Bishop A, Blacklock NJ. The influence of refined carbohydrate on urinary calcium excretion. British journal of urology. Dec 1978;50(7):459-464.

Thomas LDK, Elinder C-G, Tiselius H-G, Wolk A, Åkesson A. Ascorbic Acid Supplements and Kidney Stone Incidence Among Men: A Prospective Study. JAMA Internal Medicine. 2013;173(5):386-388.

Torricelli FC, De S, Gebreselassie S, Li I, Sarkissian C, Monga M. Type-2 diabetes and kidney stones: impact of diabetes medications and glycemic control. Urology. Sep 2014;84(3):544-548.

Tracy CR, Best S, Bagrodia A, Poindexter JR, Adams-Huet B, Sakhaee K, . . . Pearle MS. Animal protein and the risk of kidney stones: a comparative metabolic study of animal protein sources. J Urol. Jul 2014;192(1):137-141.

Trinchieri A. Diet and renal stone formation. Minerva medica. Feb 2013;104(1):41-54.

Trinchieri A, Boccafoschi C, Chisena S, De Angelis M, Seveso M. [Study of the diuretic efficacy and tolerability of therapy with Rocchetta mineral water in patients with recurrent calcium kidney stones]. Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica / Associazione ricerche in urologia. Apr 1999;71(2):121-124.

Trinchieri A, Lizzano R, Bernardini P, Nicola M, Pozzoni F, Romano AL, . . . 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. Sep 2002;34 Suppl 2:S160-163.

UCKSETP. University of Chicago Kidney Stone Evaluation and Treatment Program. Overview: Kidney Stone Causes, Treatment and Prevention. Copyright 2015. Accessed 9/16/2015.

UMICH. University of Michigan. Dietary Changes to Prevent Calcium Oxalate Stones. Accessed 7/31/2015.

UMMC. University of Maryland Medical Center. Health Information: Medical Reference Guide: Kidney Stones. Available at Last updated 06/25/2013. Accessed 04/20/15.

UMMC. University of Maryland Medical Center. Medical Reference Guide: Animation Pages: Kidney Stones. Available at: Last updated 4/14/2014. Accessed 4/14/2015.

Urivetzky M, Kessaris D, Smith AD. Ascorbic acid overdosing: a risk factor for calcium oxalate nephrolithiasis. J Urol. 1992;147(5):1215-1218.

Vicentini FC, Gomes CM, Danilovic A, Neto EA, Mazzucchi E, Srougi M. Percutaneous nephrolithotomy: Current concepts. Indian journal of urology : IJU : journal of the Urological Society of India. Jan 2009;25(1):4-10.

Wong YV, Cook P, Somani BK. The association of metabolic syndrome and urolithiasis. International journal of endocrinology. 2015;2015:570674.

Xu H, Zisman AL, Coe FL, Worcester EM. Kidney stones: an update on current pharmacological management and future directions. Expert opinion on pharmacotherapy. Mar 2013;14(4):435-447.

Yamaoka T, Itakura M. [Metabolism of purine nucleotides and the production of uric acid]. Nihon rinsho. Japanese journal of clinical medicine. Dec 1996;54(12):3188-3194.

Yasui T, Tanaka H, Fujita K, Iguchi M, Kohri K. Effects of eicosapentaenoic acid on urinary calcium excretion in calcium stone formers. European urology. May 2001;39(5):580-585.

Zerwekh JE, Odvina CV, Wuermser LA, Pak CY. Reduction of renal stone risk by potassium-magnesium citrate during 5 weeks of bed rest. J Urol. Jun 2007;177(6):2179-2184.

Zhai W, Zheng J, Yao X, Peng B, Liu M, Huang J, . . . Xu Y. Catechin prevents the calcium oxalate monohydrate induced renal calcium crystallization in NRK-52E cells and the ethylene glycol induced renal stone formation in rat. BMC complementary and alternative medicine. 2013;13:228.

Zhang F, Lau SS, Monks TJ. The cytoprotective effect of N-acetyl-L-cysteine against ROS-induced cytotoxicity is independent of its ability to enhance glutathione synthesis. Toxicological sciences : an official journal of the Society of Toxicology. Mar 2011;120(1):87-97.

Zhu W, Xu YF, Feng Y, Peng B, Che JP, Liu M, Zheng JH. Prophylactic effects of quercetin and hyperoside in a calcium oxalate stone forming rat model. Urolithiasis. Dec 2014;42(6):519-526.

Ziaee SA, Moradi A, Fateh M, Moghaddam SM. Sleep posture and unilateral renal stone formation. Scand J Urol Nephrol. 2008;42(6):551-554.

Zimmermann DJ, Voss S, von Unruh GE, Hesse A. Importance of magnesium in absorption and excretion of oxalate. Urol Int. 2005;74(3):262-267.

Zuckerman JM, Assimos DG. Hypocitraturia: pathophysiology and medical management. Rev Urol. 2009;11(3):134-44.

Zwolinska D, Medynska A, Kilis-Pstrusinska K. [Hyperuricosuria in children]. Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego. Apr 2000;8(46):179-180.