Nephrolithiasis (kidney stones) develops when conditions are present to cause supersaturation of urine, crystal formation, and aggregation of those crystals into a sizable mass. Stones can develop anywhere along the urinary tract. Kidney stones are common in Western societies; more than 10% of Americans will develop a symptomatic kidney stone during their lifetime.[1] The rate of recurrence over 5 years is estimated to be as high as 35-50%.[2]

The 5 major stone compositions are calcium oxalate, calcium phosphate, magnesium ammonium phosphate (struvite), uric acid, and cystine. Calcium-based stones are the most common, causing more than 75% of cases; calcium oxalate is the most common type overall. Struvite stones can form when certain urease-producing bacteria are present in the urinary tract.

Most often, stones are due to increased concentrations of stone-forming material in the urine, either from increased excretion or decreased urinary volume. Stone formation occurs when a stone-forming material becomes supersaturated in the urine and begins the process of crystal formation.

Many stones are asymptomatic. Large stones that become trapped in a ureter may cause severe flank pain that can radiate to the lower abdomen, groin, testicles, or perineum. Stones that lodge at the ureterovesical junction can cause lower urinary tract symptoms, including dysuria, urgency, and frequency. Nausea, vomiting, hematuria (gross and/or microscopic), and costovertebral angle tenderness may also be present, even in the absence of pain.

Risk Factors

Race and ethnicity. There is a higher incidence among White individuals compared with Asian Americans, Latinos, and Blacks.

Age. Risk increases with increasing age.

Anatomic defects of the kidneys such as horseshoe kidney may increase risk.

Gender. While traditionally more common in males, the ratio of male to female occurrence is now estimated to be almost equal.

History of nephrolithiasis. Individuals who have developed a kidney stone have an approximate 35% chance of recurrence within 5 years.[3]

Geography. Areas of elevated temperatures and high humidity appear to have an increased incidence of stone disease, likely due to population hydration status.

Socioeconomic status. Developed countries have a much higher risk of nephrolithiasis compared with developing countries, presumably due to dietary factors.

Obesity. Compared with persons at or near ideal body weight (BMI = 21-23), obese men (BMI ≥ 30) have a 33% greater risk for stone formation, while obese women have a 200% greater risk.[4] Patients who have had bariatric surgery are at risk for hyperoxaluria, which increases risk for kidney stones and kidney failure.[5]

Diet (See below).

Family history. A family history of nephrolithiasis raises risk 2-3 times.

Metabolic conditions. Insulin resistance, diabetes, obesity, cystinuria, oxaluria, gout, and hyperparathyroidism increase risk.

Urinary stasis (e.g., bladder outlet obstruction), chronic urinary tract infections, dehydration (e.g., diarrhea or malabsorption), and certain antiviral medications (e.g., indinavir, acyclovir) may also raise risk of nephrolithiasis. In addition, a guaifenesin metabolite may bind with calcium to form stones.


Clinical presentation is highly specific for kidney stones, especially in patients with a history of the condition.

Helical non-contrast CT scan is the preferred means for detecting stones and urinary tract obstructions. Abdominal (kidney-ureter-bladder) x-ray will identify many radiopaque stones but cannot detect small or radiolucent (uric acid and proteinaceous) stones or obstructions and should only be used when non-contrast CT is unavailable. The intravenous pyelogram has been largely replaced by the more sensitive CT scan, which also carries less radiation exposure.

Ultrasound and, rarely, magnetic resonance urography, are imaging options for patients who should avoid radiation (e.g., pregnant women).

Urinalysis will usually reveal hematuria. Sediment examination may reveal pathognomonic crystals, and pH may give clues about etiology. Twenty-four–hour urine collections (for creatinine, calcium, phosphorus, oxalate, uric acid, cystine, citrate) on 2 occasions, after complete resolution and recovery from the acute event and resultant treatments, can aid diagnosis.

A chemistry panel that includes calcium and uric acid may help reveal etiology (e.g., hyperuricemia and hyperparathyroidism). Renal function should be assessed as urinary tract obstruction can lead to acute renal failure.

If a stone is passed, it should be sent to the laboratory for analysis.


Immediate urologic attention is necessary for patients who present with fever, renal failure, intractable pain, persistent nausea, or signs and symptoms consistent with a systemic inflammatory response.

Small (< 5 mm) stones often pass spontaneously. While increased fluid intake facilitates passage, there is conflicting evidence for medical expulsive therapy (see tamsulosin).

Selective alpha-blockers (e.g., tamsulosin) or calcium channel blockers (e.g., nifedipine), with or without the addition of steroids, also may facilitate stone passage. However, a recent multicenter study found no significant difference in time to stone passage or analgesic use or pain in patients with stones ≤ 10mm managed medically with tamsulosin or nifedipine.[6]

Nonsteroidal anti-inflammatory drugs (e.g., indomethacin, ketorolac) and/or narcotics may be administered for pain; however, NSAIDs may increase bleeding risk following ureteroscopy or shock wave lithotripsy.

About 10-20% of stones require surgical removal. Minimally invasive surgical techniques include shock wave lithotripsy, percutaneous nephrolithotomy, and ureteroscopy. Open renal and ureteral surgery is necessary in about 1% of cases.

Extracorporeal shock wave lithotripsy is the treatment of choice for proximal renal or ureteral calculi. For the majority of middle and distal ureteral stones, ureteroscopy is preferred. This method can also be used to manage proximal ureteral and intrarenal calculi, as well as for ureteral stones that have failed shock wave lithotripsy. Nephrolithotomy is as effective as open surgery and is generally indicated for large or complex stones and cystine or monohydrate calcium stones, which are relatively resistant to lithotripsy.

Pharmacologic treatment and diet or lifestyle modifications are recommended in most cases to prevent recurrence of stones and may be specific to stone composition.

Nutritional Considerations

The incidence of kidney stones increases with animal protein intake, obesity, and poor fluid intake. Oxalates appear to be problematic primarily in persons with low calcium intake, and a vegetarian diet may offer significant protection against stone formation.

In observational studies, the following factors are associated with reduced risk:

A high fluid intake. Published guidelines suggest that daily water intake should be high enough to achieve at least 2.5 L of urine volume in order to prevent kidney stones. In a recent meta-analysis, when compared with an intake of 1,500 m/d, consumption of more than 2,000 mL of water intake per day reduced the risk of first kidney stone occurrence by roughly 8% and the highest intake (3,100 mL) was associated with a 26% reduction of risk.[7]

A healthy weight. The increase in the prevalence of kidney stones has paralleled that of obesity. The insulin resistance that occurs in obesity is associated with a reduction in renal ammonium production and low urinary pH, which could lead to the development of both uric acid stones and calcium oxalate stones.[8] The Women’s Health Initiative Study found that nephrolithiasis risk increased incrementally with BMI.[9] A study of medical claims data from nearly 100,000 individuals found that obesity (BMI > 30 kg/m2) was associated with a significantly greater likelihood of being diagnosed with a kidney stone.[10]

Bariatric surgery may increase the likelihood of stones. A review of weight loss surgeries found that Roux-en-Y gastric bypass causes a 30% reduction in urine volume, a 40% reduction in urinary citrate, and 50% increase in urinary oxalate, and increases stone incidence two-fold in non-stone formers (8.5%) and four-fold in patients with previous stone history (16.7%).[11]

Reducing intake of animal protein and sodium. Diets high in animal protein are associated with increased risk of stone formation; conversely, protein restriction causes a reduction of urinary calcium oxalate and urate.[12] Compared with individuals eating 50 g or less of animal protein per day, those eating the most (77 g or more) had a 33% higher risk for kidney stones.[13] A diet restricted in animal protein and sodium, when compared with a standard (low-calcium) diet used for prevention of calcium oxalate stone formation, reduces the risk for stone recurrence by half. A recent Cochrane review concluded that adherence to low protein and low salt diets with normal calcium intakes may also reduce the numbers of stone recurrences in people with idiopathic hypercalciuria.[14]

Limiting oxalates. American Urological Association guidelines recommend that clinicians counsel patients with calcium oxalate stones and relatively high urinary oxalate to limit intake of oxalate-rich foods and maintain normal calcium consumption.[15] However, a recent review of diets that are considered optimal for prevention of nephrolithiasis concluded that the benefits of oxalate restriction are unproven, except for bariatric surgery patients.[16]

Calcium from foods (versus supplements). Calcium intake from foods lowers the risk for calcium oxalate stones presumably because calcium binds oxalates within the intestinal tract. Oxalate absorption decreases as calcium intakes increase over a range of 200-1,200 mg per day.[17][18] Individuals consuming the greatest amount of calcium from foods have about a 30% lower risk for stone formation compared with persons consuming the lowest amounts.[19] Current evidence does not suggest that calcium supplements significantly increase the risk for nephrolithiasis; nevertheless, it has been suggested these should be taken with rather than between meals in order to minimize risk.[20]

Limiting soft drinks. Sugar-sweetened drinks, including sodas and fruit punch, appear to increase the risk for kidney stones. In a study of 194,095 participants followed for more than 8 years, individuals who consumed the highest amount of sugar-sweetened cola had a 23% higher risk of developing kidney stones, compared with those consuming the lowest amount. Those who consumed the highest amount of sugar-sweetened non-cola beverages had a 33% higher risk of developing kidney stones compared with those consuming the least. The increased risk may be due to high fructose corn syrup, which increases urinary excretion of calcium, oxalate, and uric acid.[21] Previous research found that patients who avoid colas and other phosphoric acid–containing beverages have a 15% lower rate of stone recurrence than those who continue to consume these beverages.[22] Coffee, tea, and orange juice are associated with significantly lower risk.[23][24]

Plant-based diets. The risk for stone formation is 40-60% lower in individuals following vegetarian diets for a number of reasons.[25] These include the absence of animal protein and the presence of phytic acid, which forms insoluble complexes with calcium in the intestinal tract and inhibits crystal formation in the urine. Higher fruit and vegetable intakes, which increase urine volume, pH, potassium, magnesium, citrate, and other stone inhibitors, decrease the supersaturation of calcium oxalate and uric acid overall.[9]

Avoidance of high-dose vitamin C. In a study of over 150,000 health professionals followed for more than 11 years, the highest intakes of a combination of both dietary and supplemental vitamin C were associated with a nearly 20% greater risk for kidney stones in men only.[26] Similarly, in the Cohort of Swedish Men study involving nearly 50,000 individuals, taking vitamin C supplements on a daily basis was associated with a significantly greater risk for kidney stones compared with less than daily supplementation.[27]

Dietary citrates. Citrates inhibit the formation of calcium oxalate stones by binding to calcium and interfering with calcium oxalate crystallization. However, hypocitraturia is common, found in 20% of stone formers, and increases the risk of stones.[28] Citrate supplementation (e.g., potassium citrate or potassium-magnesium citrate) is commonly prescribed for these patients. Gastrointestinal disturbances may limit compliance and benefit.[29][30] A review of strategies for reduction of risk factors for kidney stones concluded that an increased intake of fruit and vegetables (excluding those with high oxalate content) increases citrate excretion and provides significant protection against the risk of stone formation.[12]

Alcohol. A recent meta-analysis found that the amount of alcohol found in one standard drink consumed daily was associated with a 20% lower risk, compared with abstinence,[7] but the risks of alcohol use must also be taken into consideration.


See Basic Diet Orders chapter.

For patients with suspected or documented oxalate stones, consult with registered dietitian for instructions on how to follow a low-oxalate, high-magnesium diet. Avoid vitamin C supplements over 1,000 mg/d.

Consume ≥ 2.5 L of fluid (mostly water) per day.

What to Tell the Family

The risk of kidney stones is influenced by dietary factors, particularly high intake of animal protein and salt, along with low fluid consumption. Family members can help the patient in making diet changes and may benefit from these changes themselves. It is helpful to avoid animal protein and oxalate-containing foods, get adequate intake of calcium-rich foods at mealtime to reduce oxalate absorption, and drink adequate fluids.


  1. Scales CD, Smith AC, Hanley JM, et al. Prevalence of kidney stones in the United States. Eur Urol. 2012;62(1):160-5.  [PMID:22498635]
  2. Tiselius HG. Epidemiology and medical management of stone disease. BJU Int. 2003;91(8):758-67.  [PMID:12709088]
  3. Tseng TY, Preminger GM. Kidney stones. Am Fam Physician. 2013;87:441-443.
  4. Taylor EN, Stampfer MJ, Curhan GC. Obesity, weight gain, and the risk of kidney stones. JAMA. 2005;293(4):455-62.  [PMID:15671430]
  5. Asplin JR, Coe FL. Hyperoxaluria in kidney stone formers treated with modern bariatric surgery. J Urol. 2007;177(2):565-9.  [PMID:17222634]
  6. Pickard R, Starr K, MacLennan G, et al. Medical expulsive therapy in adults with ureteric colic: a multicentre, randomised, placebo-controlled trial. Lancet. 2015;386(9991):341-9.  [PMID:25998582]
  7. Xu C, Zhang C, Wang XL, et al. Self-Fluid Management in Prevention of Kidney Stones: A PRISMA-Compliant Systematic Review and Dose-Response Meta-Analysis of Observational Studies. Medicine (Baltimore). 2015;94(27):e1042.  [PMID:26166074]
  8. Kabeya Y, Kato K, Tomita M, et al. Associations of insulin resistance and glycemic control with the risk of kidney stones. Intern Med. 2012;51(7):699-705.  [PMID:22466823]
  9. Sorensen MD, Chi T, Shara NM, et al. Activity, energy intake, obesity, and the risk of incident kidney stones in postmenopausal women: a report from the Women's Health Initiative. J Am Soc Nephrol. 2014;25(2):362-9.  [PMID:24335976]
  10. Semins MJ, Shore AD, Makary MA, et al. The association of increasing body mass index and kidney stone disease. J Urol. 2010;183(2):571-5.  [PMID:20018330]
  11. Canales BK, Hatch M. Kidney stone incidence and metabolic urinary changes after modern bariatric surgery: review of clinical studies, experimental models, and prevention strategies. Surg Obes Relat Dis. 2014;10(4):734-42.  [PMID:24969092]
  12. Prezioso D, Strazzullo P, Lotti T, et al. Dietary treatment of urinary risk factors for renal stone formation. A review of CLU Working Group. Arch Ital Urol Androl. 2015;87(2):105-20.  [PMID:26150027]
  13. Curhan GC, Willett WC, Rimm EB, et al. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med. 1993;328(12):833-8.  [PMID:8441427]
  14. Escribano J, Balaguer A, Roqué i Figuls M, et al. Dietary interventions for preventing complications in idiopathic hypercalciuria. Cochrane Database Syst Rev. 2014.  [PMID:24519664]
  15. Pearle MS, Goldfarb DS, Assimos DG, et al. Medical management of kidney stones: AUA guideline. J Urol. 2014;192(2):316-24.  [PMID:24857648]
  16. Heilberg IP, Goldfarb DS. Optimum nutrition for kidney stone disease. Adv Chronic Kidney Dis. 2013;20(2):165-74.  [PMID:23439376]
  17. Curhan GC, Willett WC, Speizer FE, et al. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Intern Med. 1997;126(7):497-504.  [PMID:9092314]
  18. von Unruh GE, Voss S, Sauerbruch T, et al. Dependence of oxalate absorption on the daily calcium intake. J Am Soc Nephrol. 2004;15(6):1567-73.  [PMID:15153567]
  19. 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. J Am Soc Nephrol. 2004;15(12):3225-32.  [PMID:15579526]
  20. Sorensen MD. Calcium intake and urinary stone disease. Transl Androl Urol. 2014;3(3):235-40.  [PMID:26816771]
  21. Ferraro PM, Taylor EN, Gambaro G, et al. Soda and other beverages and the risk of kidney stones. Clin J Am Soc Nephrol. 2013;8(8):1389-95.  [PMID:23676355]
  22. Shuster J, Jenkins A, Logan C, et al. Soft drink consumption and urinary stone recurrence: a randomized prevention trial. J Clin Epidemiol. 1992;45(8):911-6.  [PMID:1624973]
  23. Curhan GC, Willett WC, Speizer FE, et al. Beverage use and risk for kidney stones in women. Ann Intern Med. 1998;128(7):534-40.  [PMID:9518397]
  24. Curhan GC, Willett WC, Rimm EB, et al. Prospective study of beverage use and the risk of kidney stones. Am J Epidemiol. 1996;143(3):240-7.  [PMID:8561157]
  25. Robertson WG, Peacock M, Marshall DH. Prevalence of urinary stone disease in vegetarians. Eur Urol. 1982;8(6):334-9.  [PMID:7140784]
  26. Ferraro PM, Curhan GC, Gambaro G, et al. Total, Dietary, and Supplemental Vitamin C Intake and Risk of Incident Kidney Stones. Am J Kidney Dis. 2016;67(3):400-7.  [PMID:26463139]
  27. Thomas LD, Elinder CG, Tiselius HG, et al. Ascorbic acid supplements and kidney stone incidence among men: a prospective study. JAMA Intern Med. 2013;173(5):386-8.  [PMID:23381591]
  28. Reynolds TM. ACP Best Practice No 181: Chemical pathology clinical investigation and management of nephrolithiasis. J Clin Pathol. 2005;58(2):134-40.  [PMID:15677531]
  29. Kang DE, Sur RL, Haleblian GE, et al. Long-term lemonade based dietary manipulation in patients with hypocitraturic nephrolithiasis. J Urol. 2007;177(4):1358-62; discussion 1362; quiz 1591.  [PMID:17382731]
  30. Jendle-Bengten C, Tiselius HG. Long-term follow-up of stone formers treated with a low dose of sodium potassium citrate. Scand J Urol Nephrol. 2000;34(1):36-41.  [PMID:10757268]
  31. Borghi L, Schianchi T, Meschi T, et al. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med. 2002;346(2):77-84.  [PMID:11784873]
Last updated: July 31, 2023