Kidney Stones

Treatment and Prevention of Kidney Stones: An Update

Kidney Stones | Johns Hopkins Medicine

1. Long LO, Park S. Update on nephrolithiasis management. Minerva Urol Nefrol. 2007;59(3):317–325….

2. Acar B, Inci Arikan F, Emeksiz S, Dallar Y. Risk factors for nephrolithiasis in children. World J Urol. 2008;26(6):627–630.

3. Sas DJ, Hulsey TC, Shatat IF, Orak JK. Increasing incidence of kidney stones in children evaluated in the emergency department. J Pediatr. 2010;157(1):132–137.

4. Ross AE, Handa S, Lingeman JE, Matlaga BR. Kidney stones during pregnancy: an investigation into stone composition. Urol Res. 2008;36(2):99–102.

5. Rule AD, Bergstralh EJ, Melton LJ III, Li X, Weaver AL, Lieske JC. Kidney stones and the risk for chronic kidney disease. Clin J Am Soc Nephrol. 2009;4(4):804–811.

6. Milliner DS, Murphy ME. Urolithiasis in pediatric patients. May Clin Proc. 1993;68:241.

7. Costa-Bauza A, Ramis M, Montesinos V, et al. Type of renal calculi: variation with age and sex. World J Urol. 2007;25(4):415–21.

8. Scholz D, Schwille PO, Ulbrich D, Bausch WM, Sigel A. Comparison of renal stones and their frequency in a stone clinic: relationship to parameters of mineral metabolism in serum and urine. Urol Res. 1979;7(3):161–70.

9. Pietrow PK, Karellas ME. Medical management of common urinary calculi. Am Fam Physician. 2006;74(1):86–94.

10. Preminger GM, Tiselius HG, Assimos DG, et al.; EAU/AUA Nephrolithiasis Guideline Panel. 2007 guideline for the management of ureteral calculi. J Urol. 2007;178(6):2418–2434.

11. Coe FL, Evan AP, Worcester EM, Lingeman JE. Three pathways for human kidney stone formation. Urol Res. 2010;38(3):147–160.

12. Matlaga BR, Williams JC Jr, Kim SC, et al. Endoscopic evidence of calculus attachment to Randall's plaque. J Urol. 2006;175(5):1720–1724.

13. Singh A, Alter HJ, Littlepage A. A systematic review of medical therapy to facilitate passage of ureteral calculi. Ann Emerg Med. 2007;50(5):552–563.

14. Dellabella M, Milanese G, Muzzonigro G. Medical-expulsive therapy for distal ureterolithiasis: randomized prospective study on role of corticosteroids used in combination with tamsulosinsimplifited treatment regimen and health-related quality of life. Urology. 2005;66(4):712–715.

15. Paige NM, Nagami GT. The top 10 things nephrologists wish every primary care physician knew. Mayo Clin Proc. 2009;84(2):180–186.

16. Saltel E, Angel JB, Futter NG, Walsh WG, O'Rourke K, Mahoney JE. Increased prevalence and analysis of risk factors for indinavir nephrolithiasis. J Urol. 2000;164(6):1895–1897.

17. Sörgel F, Ettinger B, Benet LZ. The true composition of kidney stones passed during triamterene therapy. J Urol. 1985;134(5):871–873.

18. Topamax (topiramate). DailyMed. Accessed December 30, 2010.

19. Chopra N, Fine PL, Price B, Atlas I. Bilateral hydronephrosis from ciprofloxacin induced crystalluria and stone formation. J Urol. 2000;164(2):438.

20. Siegel WH. Unusual complication of therapy with sulfamethoxazoletrimethoprim. J Urol. 1977;117(3):397.

21. Dick WH, Lingeman JE, Preminger GM, Smith LH, Wilson DM, Shirrell WL. Laxative abuse as a cause for ammonium urate renal calculi. J Urol. 1990;143(2):244–247.

22. Sterrett SP, Penniston KL, Wolf JS Jr, Nakada SY. Acetazolamide is an effective adjunct for urinary alkalization in patients with uric acid and cystine stone formation recalcitrant to potassium citrate. Urology. 2008;72(2):278–281.

23. Welch BJ, Graybeal D, Moe OW, Maalouf NM, Sakhaee K. Biochemical and stone-risk profiles with topiramate treatment. Am J Kidney Dis. 2006;48(4):555–563.

24. Curhan GC. Epidemiology of stone disease. Urol Clin North Am. 2007;34(3):287–293.

25. Gambaro G, Favaro S, D'Angelo A. Risk for renal failure in nephrolithiasis. Am J Kidney Dis. 2001;37(2):233–243.

26. American Society of Nephrology. Chronic kidney disease. Accessed April 12, 2011.

27. Swartz MA, Lydon-Rochelle MT, Simon D, Wright JL, Porter MP. Admission for nephrolithiasis in pregnancy and risk of adverse birth outcomes. Obstet Gynecol. 2007;109(5):1099–1104.

28. Hesse A, Siener R, Heynck H, Jahnen A. The influence of dietary factors on the risk of urinary stone formation. Scanning Microsc. 1993;7(3):1119–1127.

29. Marangella M, Bagnis C, Bruno M, Vitale C, Petrarulo M, Ramello A. Crystallization inhibitors in the pathophysiology and treatment of nephrolithiasis. Urol Int. 2004;72(suppl 1):6–10.

30. Serio A, Fraioli A. An observational and longitudinal study on patients with kidney stones treated with Fiuggi mineral water [in Italian]. Clin Ter. 1999;150(3):215–219.

31. Parks JH, Coe FL. Evidence for durable kidney stone prevention over several decades. BJU Int. 2009;103(9):1238–1246.

32. Borghi L, Meschi T, Amato F, Briganti A, Novarini A, Giannini A. Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study. J Urol. 1996;155(3):839–843.

33. Takeuchi H, Ueda M, Satoh M, Yoshida O. Effects of dietary calcium, magnesium and phosphorus on the formation of struvite stones in the urinary tract of rats. Urol Res. 1991;19(5):305–308.

34. Jarrar K, Boedeker RH, Weidner W. Struvite stones: long term follow up under metaphylaxis. Ann Urol (Paris). 1996;30(3):112–117.

35. Siva S, Barrack ER, Reddy GP, et al. A critical analysis of the role of gut Oxalobacter formigenes in oxalate stone disease. BJU Int. 2009;103(1):18–21.

36. Hoppe B, Beck B, Gatter N, et al. Oxalobacter formigenes: a potential tool for the treatment of primary hyperoxaluria type 1. Kidney Int. 2006;70(7):1305–1311.

37. Batmanghelidj F, Kohlstadt I. Water: a driving force in the musculoskeletal system. In: Scientific Evidence for Musculoskeletal, Bariatric and Sports Nutrition. Boca Raton, Fla.: Taylor & Francis; 2006:127–135.

38. Livingston EH, Kohlstadt I. Simplified resting metabolic rate-predicting formulas for normal-sized and obese individuals. Obes Res. 2005;13(7):1255–1262.

39. Ekeruo WO, Tan YH, Young MD, et al. Metabolic risk factors and the impact of medical therapy on the management of nephrolithiasis in obese patients. J Urol. 2004;172(1):159–163.

40. 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. 2010;183(6):2244–2248.

41. Maalouf NM, Cameron MA, Moe OW, Sakhaee K. Metabolic basis for low urine pH in type 2 diabetes. Clin J Am Soc Nephrol. 2010;5(7):1277–1281.

42. Breslau NA, Brinkley L, Hill KD, Pak CY. Relationship of animal protein-rich diet to kidney stone formation and calcium metabolism. J Clin Endocrinol Metab. 1988;66(1):140–146.

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

44. Choi HK, Willett W, Curhan G. Fructose-rich beverages and risk of gout in women. JAMA. 2010;304(20):2270–2278.

45. Trinchieri A, Esposito N, Castelnuovo C. Dissolution of radiolucent renal stones by oral alkalinization with potassium citrate/potassium bicarbonate. Arch Ital Urol Androl. 2009;81(3):188–191.

46. Sakhaee K, Nicar M, Hill K, Pak CY. Contrasting effects of potassium citrate and sodium citrate therapies on urinary chemistries and crystallization of stone-forming salts. Kidney Int. 1983;24(3):348–352.

47. Pizzarelli F, Peacock M. Effect of chronic administration of ammonium sulfate on phosphatic stone recurrence. Nephron. 1987;46(3):247–252.


Kidney stones

Kidney Stones | Johns Hopkins Medicine

Kidney stones (also called renal stones or urinary stones) are small, hard deposits that form in one or both kidneys; the stones are made up of minerals or other compounds found in urine. Kidney stones vary in size, shape, and color.

To be cleared from the body (or “passed”), the stones need to travel through ducts that carry urine from the kidneys to the bladder (ureters) and be excreted. Depending on their size, kidney stones generally take days to weeks to pass the body.

Kidney stones can cause abdominal or back pain (known as renal colic). Renal colic usually begins sporadically but then becomes constant and can lead to nausea and vomiting. The site of pain can change as the stone moves through the urinary tract.

Some small stones pass through the kidney and urinary tract with little discomfort, while larger ones can block the flow of urine and impair kidney function. Kidney stones can also result in blood in the urine (hematuria) or kidney or urinary tract infections.

Unusually large stones or stones that are difficult to pass can be medically removed.

Although there are many types of kidney stones, four main types are classified by the material they are made of. Up to 75 percent of all kidney stones are composed primarily of calcium.

Stones can also be made up of uric acid (a normal waste product), cystine (a protein building block), or struvite (a phosphate mineral). Stones form when there is more of the compound in the urine than can be dissolved.

This imbalance can occur when there is an increased amount of the material in the urine, a reduced amount of liquid urine, or a combination of both.

People are most ly to develop kidney stones between ages 40 and 60, though the stones can appear at any age. Research shows that 35 to 50 percent of people who have one kidney stone will develop additional stones, usually within 10 years of the first stone.

In the United States, 9 percent of women and 19 percent of men develop kidney stones in their lifetime. Caucasians are more ly to develop kidney stones than African Americans.

Genetic changes can increase the risk of developing kidney stones, often acting in combination with a variety of environmental and lifestyle factors. Most genes involved in the condition are important for transmitting chemical signals from outside cells to inside cells or transporting materials in and cells.

These processes help regulate the levels of various materials within cells, including the minerals and compounds that make up kidney stones. Changes in these genes can alter the levels of these materials in cells, leading to an imbalance of minerals and compounds in urine.

As a result, the lihood of stone formation increases.

A key factor that contributes to the development of kidney stones is too little water in the body (dehydration). When a person is dehydrated, they excrete less water in their urine, so the urine becomes concentrated with minerals and compounds that can cluster to form stones. Eating certain foods, such as animal proteins or foods high in sodium, can increase the lihood of developing stones.

A diet deficient in calcium can increase levels of other substances that cause stone development in individuals who have a history of kidney stones. Additionally, people who take certain medications, such as diuretics, which help remove water and salt from the body through urine, or calcium antacids, which treat indigestion by neutralizing stomach acids, are more ly to develop kidney stones.

In most cases, kidney stones occur without any other health issues. However, some people develop kidney stones as part of another condition. About half of people who develop calcium stones have high levels of calcium in the urine (hypercalciuria). Hypercalciuria often runs in families.

Some other health conditions that increase the risk of kidney stones include obesity, type 2 diabetes, inflammatory bowel disease (abnormal inflammation of the intestinal walls), gout (abnormal inflammation in the joints caused by high levels of uric acid in the blood), hyperparathyroidism (overactivity of the parathyroid glands), renal tubular acidosis (kidney dysfunction that leads to too much acid in the blood), and recurrent urinary tract infections.

The inheritance pattern of kidney stones is unclear. Overall, the risk of developing this condition is greater for individuals who have a close relative (such as a parent or sibling) with the condition as compared to the general public.

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Biomarkers to diagnose serious kidney allergic reaction

Kidney Stones | Johns Hopkins Medicine

A team led by Johns Hopkins Medicine researchers says it has identified two protein biomarkers in urine that may one day be used to better diagnose acute interstitial nephritis (AIN), an underdiagnosed but treatable kidney disorder that impairs renal function in the short term and can lead to chronic kidney disease, permanent damage or renal failure if left unchecked.

The finding is reported in the May 16, 2019, issue of the Journal of Clinical Investigation Insight.

Acute interstitial nephritis is a condition marked by inflammation and swelling of the renal tubules, the tiny portals in the kidneys where blood is filtered.

As a result, the tubules cannot properly reabsorb water and useful organic substances, such as glucose and amino acids, or secrete waste products such as urea and creatinine into urine.

AIN is commonly the result of autoimmune diseases or allergic reactions to more than 100 medications, including antibiotics, pain relievers and antacids. The disease is estimated to cause 15 to 20% of all hospitalizations for acute kidney injury.

Currently, the only method of diagnosing AIN is by examining renal tissue obtained with a biopsy, putting patients at some risk from complications. Additionally, samples can sometimes be misinterpreted or yield inconclusive results.

“What has been needed is a biological diagnostic tool that is safe, easy to get and measure, simple to interpret, consistent across patient populations and most importantly, extremely accurate at identifying AIN.” says Chirag Parikh, Ph.D., director of the Division of Nephrology at Johns Hopkins University School of Medicine and senior author of the new paper.

To find such a biomarker, Parikh and his colleagues looked for a substance linked to AIN's most distinct characteristic, inflammation of the renal tubules, formally known as tubulitis.

Knowing that cytokines — proteins secreted by immune cells known as CD4+ T lymphocytes — are the agents causing inflammation of the tubules, the researchers measured the amounts of 12 urine and 10 blood plasma proteins in samples from 79 adult, biopsy-confirmed AIN patients, and compared them to the amounts in 186 adult kidney biopsy patients without an AIN diagnosis.

The results, reviewed independently by three pathologists, showed that none of the plasma biomarkers were associated with AIN, but that two proteins — tumor necrosis factor-alpha (TNF-α) and interluken-9 (IL-9) — were consistently seen in the urine of AIN patients. Neither cytokine was present in the control samples, either in plasma or urine.

“Because both cytokines are seen in allergic diseases such as atopic dermatitis and food allergies, and AIN most often is the result of an allergic response, it makes sense to consider using them as diagnostic tools,” Parikh says.

“Additionally, we knew that IL-9 leads to the accumulation of mast cells that release histamine and other chemicals that induce allergic responses, and kidney biopsies from AIN patients frequently reveal the presence of mast cells,” he adds. “This suggests that IL-9 may be the stronger link to AIN, and perhaps, the better candidate as a future predictive biomarker.”

To test the sensitivity of using IL-9 in this manner, the researchers compared its AIN-detecting ability in patients whose disease was confirmed by pathologists who evaluated biopsied material or was symptomatically diagnosed by clinicians prior to the biopsies.

“If biopsy diagnoses are considered 100% accurate, then IL-9 had a very comparable ranking of 84%, and this was significantly better than the 62 to 69% achieved by clinicians without biopsies,” Parikh says.

The next step for the research team, Parikh says, will be to verify the findings of this study in a larger group of patients and get support for the development of TNF-α and IL-9 as tools to complement AIN diagnosis by biopsy. He says the hope is that later, biomarkers can replace kidney biopsies altogether.

“Biopsy is currently the 'gold standard' for AIN diagnosis, but we believe that biomarkers will one day be a more robust, more accurate, more cost effective and more patient-friendly method,” Parikh says.

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Kidney Stones | Johns Hopkins Medicine

Nearly 1 in 4 people with diabetes will develop diabetic kidney disease. In fact, kidney disease is one of the most common complications of diabetes but can be prevented. Diabetic kidney disease does not always lead to kidney failure and dialysis. Early diagnosis and treatment are more important to prevent kidney disease from progressing.

One of the earliest signs of kidney disease is an excess amount of protein in the urine. This can be detected using a urine microalbumin test.

People with type 2 diabetes are usually screened for the early stages of kidney disease when they are first diagnosed. People with type 1 diabetes are typically screened starting 5 years after their diagnosis. After that, people with both type 1 and type 2 diabetes are then generally screened once per year.

Symptoms are rare during the mildest stages of kidney disease. As kidney disease progresses, you may notice some warning signs, such as:

  • Rise in blood pressure
  • Swelling in the hands, feet or legs
  • Loss of appetite
  • Weight loss
  • Nausea
  • Tiredness
  • Metallic taste in the mouth
  • Waking up to visit the bathroom several times at night

If your healthcare provider observes one or more of these warning signs, he or she may recommend additional tests such as urine creatinine to evaluate your kidney function. These tests can be used to measure how quickly your kidneys filter the blood to remove potential toxins, known as the ‘glomerular filtration rate’

Kidney disease is categorized into five stages both the presence of protein in the urine and the glomerular filtration rate (GFR):

Stage GFR (mL/min) Condition of the Kidneys
1 90 or Higher The kidneys function normally but the patient is at risk for kidney disease
2 60-89 Mild decline in kidney function
3 30-59 Moderate decline in kidney function
4 15-29 Severe decline in kidney function
5 14 or lower Kidney failure (end-stage)

During the earliest stages of kidney disease, you can protect your kidneys and health, in general, by:

  • Keeping your blood glucose levels at target
  • Stop smoking
  • Controlling your blood pressure and cholesterol levels with lifestyle changes or medication
  • Exercising and eating a healthy diet
  • Reducing your salt intake. Be sure to read food labels, even for foods that aren’t considered very salty!

During later stages of kidney disease, work closely with your healthcare provider to:

  • Adjust insulin doses. As kidney function worsens, you will ly need less insulin in the latest stages.
  • Reduce the doses of some of your oral medications, especially metformin and sulfonylureas
  • Avoid drugs that may harm your kidneys, such as aspirin, ibuprofen, and the contrast used in CT scans


Kidney Stones: Causes, Symptoms & Treatment

Kidney Stones | Johns Hopkins Medicine

A kidney stone is a hard mass that forms in one or both kidneys from minerals in the urine, and if large enough, can cause severe pain. In the United States, kidney stones send more than 500,000 people to the emergency room each year, according to the National Kidney Foundation.


Kidney stones form when there is not enough liquid in the urine to dilute out waste chemicals, such as calcium, oxalate and phosphorous. These waste chemicals become concentrated, and crystals begin to form, according to the National Kidney Foundation.

The most common type of kidney stones are calcium oxalate stones.

Kidney stones can vary in size, with some as small as a grain of sand, and others as large as a pea or even a golf ball, according to the National Institutes of Health (NIH).

Small stones may pass down the urinary tract and be excreted without causing symptoms. Larger stones may get stuck in the urinary tract and block the flow of urine, which can cause severe pain or bleeding, the NIH says.


People with kidney stones often seek medical care because they have severe pain in their flank (the area between the mid-back and the ribs) on one side of the body, and this pain can extend to the lower abdomen, said Dr. Michael F. Michelis, director of the division of nephrology at Lenox Hill Hospital in New York. “Stone pain is very profound,” Michelis said.

Other symptoms of kidney stones can include pain while urinating, blood in the urine, and nausea and vomiting, according to the NIH. People who think they have a kidney stone, or who have serious symptoms such as extreme pain that won't go away, fever, chills and vomiting, should see their doctor, the NIH says.

Risk factors

Men are more ly to develop kidney stones than women. People are also at increased risk for kidney stones if they've had a stone in the past, or a member of their family has had a stone. 

Other risk factors include not drinking enough water, eating a diet high in protein, sodium and sugar, being obese, or undergoing gastric bypass surgery, according to the Mayo Clinic. 

The most common time to develop kidney stones is between ages 20 and 60, according to information from The Johns Hopkins Hospital.

Kidney stones broken into smaller pieces after lithotripsy. (Image credit: Atelier_A Shutterstock)


Kidney stones can be diagnosed from a patient's symptoms and a CT scan (that combines X-rays to create a 3D image), which is usually performed in the emergency room, Michelis said.


Small kidney stones don't usually need treatment, but an individual may need to take pain medication, according to the NIH. Patients with kidney stones should also drink lots of fluids, which can help the stone to pass. Most kidney stones do not require invasive treatment, according to the Mayo Clinic. 

Large kidney stones, or stones blocking the urinary tract, may need other treatments. One treatment is called shock wave lithotripsy, during which a doctor uses a machine that produces strong vibrations known as shock waves to break the stone into small pieces so it can pass through the urinary tract.

Another treatment, called ureteroscopy, uses a special tool called a ureteroscope to view the kidney stone in the ureter — the tube that connects the kidneys to the bladder. A doctor can then remove the stone or use laser energy to break it up.

Very large stones may need surgery to remove them, Michelis said. 


Many issues of kidney stones “can be avoided by moderation of the diet and a high fluid intake,” Michelis said. The NIH recommends drinking about 2 to 3 liters, or 2 to 3 quarts, of fluid each day.

Determining the type of stone a person had — by catching the stone as it passes and having it analyzed by a lab — can help doctors understand what caused the stone, and make recommendations to prevent the condition.

If a patient is not able to catch the kidney stone, doctors can still perform urine testing (by asking a patient to collect his or her urine for a 24-hour period), and take a diet history, to determine what might be causing the stone, Michelis said.

For people who've had stones made of calcium oxalate, doctors may recommend that they avoid foods high in oxalate, such as spinach, rhubarb, nuts and wheat bran, the NIH says. 

To prevent stones made of uric acid, doctors may ask patients to reduce their protein intake, because protein is associated with the formation of uric acid in the body, Michelis said.

Reducing salt intake may also lower a person's risk of several types of kidney stones, including calcium stones. Eating too much sodium can increase the amount of calcium in the urine, Michelis said. Patients should also eat the recommended daily amount of calcium, but not an excessive amount, Michelis said.

Some drugs can help prevent kidney stones, but these drugs are typically used only if a change in diet is not effective, Michelis said.

These include diuretic drugs to prevent calcium stones and drugs to reduce the production of uric acid to prevent uric acid stones, Michelis said.

Some drugs can also reduce the acidity of the urine, Michelis said, because too much acid in the urine is a risk factor for stones made of uric acid.

This article is for informational purposes only, and is not meant to offer medical advice. 

Follow Rachael Rettner @RachaelRettner. Follow Live Science @livescience, & .

Additional reporting by Cari Nierenberg, Live Science Contributor

Additional resources


Kidney Stones

Kidney Stones | Johns Hopkins Medicine

Kidney stones are hard objects, made up of millions of tiny crystals. Most kidney stones form on the interior surface of the kidney, where urine leaves the kidney tissue and enters urinary collecting system. Kidney stones can be small, a tiny pebble or grain of sand, but often are much larger.

The job of the kidneys is to maintain the body's balance of water, minerals and salts. Urine is the product of this filtering process.

Under certain conditions, substances normally dissolved in urine such as calcium, oxalate, and phosphate, become too concentrated and can separate out as crystals.

A kidney stone develops when these crystals attach to one another, accumulating into a small mass, or stone.

Kidney stones come in a variety of mineral types.

  1. Calcium Stones: Most kidney stones are composed of calcium and oxalate. Many people who form calcium containing stones have too much calcium in their urine, a condition known as hypercalciuria. There are several reasons why hypercalciuria may occur. Some people absorb too much calcium from their intestines. Others absorb too much calcium from their bones. Still others have kidneys which do not correctly regulate the amount of calcium they release into the urine. There are some people who form calcium oxalate stones as a result of too much oxalate in the urine, a condition known as hyperoxaluria. In some cases, too much oxalate in the urine is a result of inflammatory bowel disease, such as Crohn's disease or ulcerative colitis, or other times it may be a consequence of prior intestinal surgery. Calcium phosphate stones, another kind of calcium stone, are much less common than calcium oxalate stones. For some people, calcium phosphate stones form as a result of a medical condition known as renal tubular acidosis. 
  2. Struvite Stones: Some patients form stones that are composed of a mixture of magnesium, ammonium, phosphate, and calcium carbonate, which is known as struvite. These stones form as a result of infection with certain types of bacteria that can produce ammonia. Ammonia acts to raise the pH of urine which makes it alkaline and promotes the formation of struvite. 
  3. Uric Acid Stones: Uric acid is produced when the body metabolizes protein. When the pH of urine drops below 5.5, urine becomes saturated with uric acid crystals, a condition known as hyperuricosuria. When there is too much uric acid in the urine, stones can form. Uric acid stones are more common in people who consume large amounts of protein, such as that found in red meat or poultry. People with gout can also form uric acid stones. 
  4. Cystine Stones: Cystine stones are rare, and they form only in persons with an inherited metabolic disorder that causes high levels of cystine in the urine, a condition known as cystinuria.