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Cystinuria: Treatment & Medication

Author: Chandra Shekhar Biyani, MBBS, MS, DUrol, FRCS(Urol), FEBU, Consulting Urologist, Department of Urology, Pinderfields General Hospital, UK
Coauthor(s): Jon Cartledge, MD, FRCS (Urol), Consulting Urologist, Pyrah Department of Urology, St James's University Hospital, UK
Contributor Information and Disclosures

Updated: Jun 23, 2009

Treatment

Medical Care

The foundation of cystine stone prevention is adequate hydration and urinary alkalinization. When this conservative therapy fails, the addition of thiol drugs, such as D-penicillamine, alpha-MPG, and captopril, are added to the regimen. Disappointingly few advances in the medical treatment of cystinuria have occurred over the last 10-15 years. No therapy currently addresses the underlying derangement of dibasic amino acid transport.

  • Management algorithm
    • Overall, for a patient with cystinuria who does not have a stone, first-line therapy in most cases is a conservative approach, including large-volume fluid intake (urine output >2.5 L/d), regular urine pH monitoring (urine pH level of 7.5 and <8), dietary restrictions, and urinary alkalization with potassium citrate.
    • If this standard therapy fails to achieve the urinary cystine concentration of 300 mg/L, then medical therapy with D-penicillamine, alpha-MPG, or captopril must be added.
    • Treat patients with stone disease according to the location of the stone. The expertise of a urologist and a radiologist is important for decision-making processes, and stone site and size also influence further management (see Image 7).

      Treatment algorithm for cystinuria.

      Treatment algorithm for cystinuria.

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      Treatment algorithm for cystinuria.

      Treatment algorithm for cystinuria.

  • Hydration
    • The average homozygous patient with cystinuria excretes 600-1400 mg of cystine per day. The solubility of cystine at a pH level of 7 is 250-300 mg/L. Therefore, one of the oldest and most effective cystine stone–prevention techniques is hyperdiuresis to decrease urinary cystine concentration. Early studies by Dent et al in the 1960s showed that hydration alone could prevent stone recurrence in up to a third of patients. This finding has been corroborated by more recent studies.
    • The goals of hydration therapy are urine volumes in excess of 3 L/d. This goal may require ingesting 4-4.5 L of water per day. Patients should drink 240 mL of water every hour during the day and 480 mL before retiring and at least once during the night.
    • Alkalizing beverages, such as mineral water, rich in bicarbonate and low in sodium (1500 mg HCO3/L, maximum 500 mg sodium/L), and citrus juices are preferred.
    • Patients should monitor the specific gravity of their urine using Nitrazine dipsticks, with a goal of achieving a value less than 1.010.
  • Alkalinization
    • Alkaline urine can prevent the precipitation of cystine calculi and can even aid in dissolution. Urine pH level must be more than 7.5 for stone dissolution to occur.
    • Paradoxically, a urine pH level of more than 7.5 can cause a predisposition to the formation of calcium phosphate calculi, so urine must be monitored with dipsticks to maintain a pH level of 7-7.5 for stone prevention.
    • Currently, Nitrazine paper and standard pH dipsticks have no clear color differentiations in the pH level range of 6-7.5. UriDynamics, a small company in Indianapolis, Ind, has developed a new test strip called StoneGuard II. This strip includes an additional color block at a pH level of 7.5. The colors produced are yellow-orange (pH level of 5), yellow-green (pH level of 6), green-yellow (pH level of 6.5), light green (pH level of 7), green with blue cast (pH level of 7.5), and greenish blue (pH level of 8). No interference from common medications, nutritional supplements, or blood has been observed. It also has a pad to measure specific gravity over a range of 1.000-1.030.
    • Sodium bicarbonate was used in the past but is no longer recommended as a first-line agent. The sodium ion may actually increase the amount of cystine excreted.
    • Potassium citrate is the first-line alkalinizing drug. The typical adult dose is 60-80 mEq/d divided into 3-4 doses (15-20 mL/d), titrating the dose as needed to maintain a urine pH level within the target range of 7-7.5.
    • Acetazolamide inhibits the brush-border carbonic anhydrase of the proximal convoluted tubule, thereby increasing urinary bicarbonate excretion. Acetazolamide is not widely used as a first-line drug and is of questionable efficacy.
    • With any alkalinization therapy, monitoring of urinary pH is essential.
  • Chelating agents
    • Cystine-binding and cystine-reducing agents share the ability to dissociate the cystine molecule into disulfide moieties with much higher solubilities than the parent molecule. These drugs are thiol derivatives. The treatment goal is excretion of less than 200 mg/d of urinary cystine, and this must be monitored yearly.
    • Start these agents when hydration, dietary, and alkalinization therapies fail.
    • Cystine-binding agents can dissolve cystine calculi, but this feat usually takes many months to years. They are best suited for stone prevention after surgical debulking of the stone burden, and they possibly help soften cystine stones in preparation for ESWL.
  • Penicillamine
    • Penicillamine is a first-generation chelating agent that combines with cystine to form a soluble disulfide complex (50 times more soluble than cystine), thus preventing stone formation and possibly even dissolving existing cystine stones. Three types of isomers of penicillamine are known and include D, L, and DL. Only the D form should be used clinically.
    • The effect of the drug is dose-dependent. A 250-mg/d increase in dose decreases the urinary cystine level by 75-100 mg/d. Doses of 1-2 g/d are effective in reducing the urinary cystine level to 200 mg/g of creatinine.
    • The prevalence rate of adverse reactions is approximately 50%; therefore, routine use is limited. Adverse effects include rash, arthralgia, leukopenia, gastrointestinal intolerance, and nephritic syndrome.
    • Long-term therapy may lead to vitamin B-6 (pyridoxine) deficiency; thus, vitamin B-6 supplementation (50 mg/d) is needed.
  • Alpha-mercaptopropionylglycine
    • This second-generation chelating agent is a mercaptan agent with a chemical structure and mechanism of action similar to that of D-penicillamine. It was approved by the US Food and Drug Administration in 1988.
    • Alpha-MPG has a 30% higher dissolution capacity for cystine than penicillamine.
    • The mechanism of action is based on a thiol disulfide exchange reaction similar to that of D-penicillamine.
    • The drug is not excreted in the urine, so the cyanide-nitroprusside test is an effective qualitative screening method for monitoring the control of cystinuria. A positive test result indicates the need for an increased dosage.
    • The main advantage of thiol is its lower toxicity profile. In a multicenter trial by Pak et al in 1986, 69% of subjects discontinued D-penicillamine because of adverse reactions, compared with 31% for alpha-MPG.13
  • Captopril
    • In 1987, Sloand and Izzo reported the effectiveness of captopril in the treatment of patients with cystinuria.29
    • Captopril is a thiol first-generation ACE inhibitor and has been shown to form a thiol-cysteine mixed disulfide. This complex is 200 times more soluble than cystine.
    • Newer thiol compounds, such as thiophosphate and meso-2-3-dimercaptosuccinic acid, have been used both in vitro and in a few clinical trials.
    • Captopril at doses of 75-100 mg was used in 2 patients, and cystine excretion decreased 70% and 93%. However, as reported by Sloand and Izzo, various follow-up studies have reported conflicting results.29
    • Captopril can be used to treat patients whose conditions fail to respond to standard treatment and to treat patients with cystinuria who are hypertensive.
  • Bucillamine
    • Bucillamine (Rimatil), a dithiol compound, was reported by Koide et al in 1992 and is a third-generation chelating agent available only in Japan and South Korea.30
    • Incubation of L-cystine with a specific amount of bucillamine and tiopronin (Thiola) in vitro studies showed a substantially lower amount of L-cystine in the presence of bucillamine compared with tiopronin.
    • Use of bucillamine in persons with rheumatoid arthritis showed a low toxicity profile; therefore, it is probably well tolerated by patients with cystinuria.

Surgical Care

Indications for surgery are large calculi that are unlikely to dissolve and obstructing or otherwise symptomatic calculi. Smaller stones can be monitored as part of an aggressive medical treatment plan with the hope of dissolution and/or spontaneous passage. The ultimate goal of surgery is to make the patient free of stones. While the risk of recurrence is unchanged, the time to recurrence is significantly lengthened.

Surgical options can be broadly classified into 6 modalities, including (1) ESWL, (2) retrograde endoscopic lithotripsy and extraction, (3) percutaneous nephrolithotomy, (4) multimodal therapy, (5), percutaneous nephrostomy for chemical dissolution, and (6) open surgery (urethra, bladder, ureter, kidneys).

  • Extracorporeal shockwave lithotripsy
    • ESWL is especially effective for cystine stones smaller than 1.5 cm in diameter, although overall stone-free rates are lower compared with rates for stones of other composition.
    • Because of their hardness and homogenous amino acid composition, most cystine stones require 2-3 times the usual number of shocks to adequately fragment the stone. Multiple treatments are often necessary to achieve acceptable stone-free rates.
    • When considering candidates for ESWL, some authors suggest an upper limit of 1.5 cm for upper ureteral or renal cystine calculi. As reported by Kachel et al in 1991, these authors prefer to limit ESWL to renal calculi smaller than 1 cm in diameter.31
    • ESWL is appropriate in the treatment of ureteral cystine calculi. Stones not visualized after fluoroscopy can still be opacified by either retrograde or intravenous contrast administration to allow for lithotripsy.
    • Patients taking thiol derivatives may have cystine calculi that are more fragile because the cystine is replaced by apatite in approximately 30% of cases. These calculi may be easier to treat with ESWL.
  • Retrograde endoscopic lithotripsy and extraction
    • Historically, retrograde endoscopic treatment of cystine calculi was associated with complications and a low success rate compared with stones of other composition of equal size and location in the urinary tract. This was largely due to technical limitations in scope design and the failure of electrohydraulic lithotripsy to adequately fragment stones.
    • Currently, a retrograde approach is suitable for mid-to-distal ureteral cystine calculi when using high-energy modalities such as holmium:YAG laser or pneumatic shock devices (eg, Lithoclast). Smaller proximal ureteral calculi may also be treated in a retrograde fashion.
    • The role of retrograde treatment of renal calculi and large proximal stones is less clear, although ESWL and percutaneous surgery are generally preferred for larger stones. However, one study reports 5 of 6 patients with renal calculi 1.5-3 cm in diameter who were successfully treated via a retrograde approach with intracorporeal electrohydraulic lithotripsy.
  • Percutaneous nephrolithotomy
    • Percutaneous nephrolithotomy is the criterion standard for cystine renal calculi larger than 1-1.5 cm in diameter and for calculi for which ESWL or retrograde surgery has failed.
    • Ultrasonic lithotripsy readily fragments most cystine stones, although re-treatment rates are still approximately 50% compared with approximately 15% for other calculi.
    • Stone-free rates after multiple treatments range from 40%-86%, although recurrence rates are high, approaching 50%-70% at 5-year follow-up despite postoperative medical management.
  • Multimodal therapy
    • For large cystine stone burdens, such as occurs with full staghorn calculi, multimodal therapy may help achieve better stone-free rates.
    • So-called sandwich therapy involves initial percutaneous ultrasonic lithotripsy followed by ESWL and then repeat ultrasonic lithotripsy or flexible nephroscopy and laser lithotripsy.
  • Percutaneous nephrostomy for chemical dissolution
    • Direct irrigation of renal calculi with chemodissolution agents through a percutaneous nephrostomy tube was successful in treating a limited number of patients in the late 1970s and early 1980s.
    • The 2 most commonly used agents were acetylcysteine (Mucomyst) and tromethamine-E (THAM-E). Acetylcysteine creates soluble disulfide complexes with cystine, similar to the action of D-penicillamine. In addition, percutaneous administration of alkalinizing agents can create a pronounced alkaline milieu. A solution containing 60 mL of a 20% solution of N -acetylcysteine and 300 mEq of sodium bicarbonate per liter of saline is recommended. Tromethamine-E is an organic amine buffer with a pH level of 10.2.
    • Treatment times range from weeks to months. Given the extended treatment times, relatively low success rates, and success of ESWL and percutaneous nephrolithotomy, this modality is rarely used today. Some urologists may still use chemodissolution to help achieve stone-free status in patients with fragments remaining after percutaneous nephrolithotomy or ESWL or for patients unable to tolerate surgery.
  • Open surgery
    • Given the success of percutaneous nephrolithotomy, ESWL, and endoscopic retrograde approaches, open surgery is not indicated as first-line therapy for cystine calculi anywhere in the kidneys or ureter, with rare exceptions. Large bladder calculi may be amenable to open surgery, but these stones can also be treated with laser or electrohydraulic lithotripsy.
    • Ureteral substitution with small intestine has been reported in highly select cases.

Consultations

Treatment of the patient with cystinuria requires close cooperation between the urologist and the nephrologist. Maintaining high diuresis of at least 3 L/d, regularly distributed throughout the night and day, even when sulfhydryl compounds are given, appears to be the major factor predictive of therapeutic success. Regular clinical, radiological, and biochemical surveillance appears to be of primary importance to maintain good long-term compliance with medical treatment.

Diet

Cystine is formed during the metabolism of methionine; therefore, a diet low in methionine is effective. To be effective, dietary methionine must be reduced to 1 g/d. Unfortunately, a primarily vegetarian diet is generally not accepted by patients. Thus, a well-balanced mixed diet with relatively low-protein content (0.8 g protein/kg body weight/d) is recommended. Dietary restriction of methionine found in animal proteins such as milk, eggs, cheese, and fish may be helpful.

Cystine excretion increases with high-sodium intake. Processed foods contain large amounts of sodium chloride and are best avoided.

  • Methionine: Instruct patients to avoid foods with very high methionine content, including stockfish and eggs, and to reduce their consumption of meat, fish, poultry, and cheese. One study reported decreased cystine production (by approximately 500 µmol/d) with reduced methionine intake.
  • Low-sodium diet: Reducing sodium intake from 300 mmol/d to 50 mmol/d can decrease cystine excretion by 650 µmol/d (156 mg/d).
  • Glutamine: A series from 1979 reported by Miyagi et al indicated reduced cystine excretion with oral or intravenous glutamine. However, this effect has not been duplicated in other studies.32
  • Dietary guidelines for patients
    • Eat only small amounts of protein-rich foods such as meat, fish, sausages, eggs, cheese, and soybeans.
    • Consume foods with a low-protein content, such as fruits, vegetables, salads, and cereals.
    • Limit additional salt during meals; limit canned foods, smoked foods, and pickled foods.
    • Increase dietary fiber intake.

Medication

Without medical therapy, patients with cystinuria are certain to develop new calculi. Strategies for stone prevention and dissolution include adequate urine output, urinary alkalinization, and use of thiol derivatives.

The goal for urine output is 3 L/d. In the past, sodium bicarbonate was used for alkalinization, but potassium citrate is preferred today to help limit dietary sodium intake. Thiol derivatives are used when calculi recur despite adequate hydration and alkalinization. These agents dissociate the cystine homodimer and create a new disulfide molecule that is more soluble in urine.

D-penicillamine has been used the longest in cystine stone prevention but is the least well-tolerated. More than 50%-70% of patients stop taking the drug because of its adverse effects. Alpha-MPG acts in a manner similar to that of D-penicillamine, but its adverse effects are less severe and patient compliance approaches 70%. Captopril is another thiol derivative that decreases urinary excretion of cystine. Although well tolerated, the clinical efficacy of captopril for preventing new stones is still being evaluated.

Urinary alkalinization agents

Potassium citrate is metabolized to bicarbonates, which increase urinary pH levels by increasing the excretion of free bicarbonate ions without producing systemic alkalosis when administered in recommended doses. A rise in urinary pH levels increases the solubility of cystine in the urine. Raise the urine pH level to 7-7.5 to make cystine more soluble.


Potassium citrate (Bicitra, Citrolith, Oracit, Polycitra Syrup, Polycitra-K)

Maintains urine pH level of 7-7.6.

Adult

15-20 mL PO qid

Pediatric

Not established

Caution in patients with renal impairment and hypertension

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Gastric irritation may occur; tabs should always be well diluted with water; gastric effects may be minimized by taking with or after meals; hyperkalemia


Potassium bicarbonate (Sando-K, Kloref, Kloref-S)

Because solubility of cystine increases with pH level of >7.5, urinary alkalization is successful. One gram of potassium bicarbonate provides 10 mEq of potassium.

Adult

1-2 mEq/kg/d PO

Pediatric

Appropriate studies on the relationship of age to the effects of citrates have not been performed in pediatric populations; however, no pediatric-specific problems have been documented to date

ACE inhibitors, cyclosporin, and potassium-sparing diuretics cause increased risk of hyperkalemia

Documented hypersensitivity, hyperkalemia or conditions predisposing to hyperkalemia; serum potassium >5 mmol/L; hypochloremia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Diarrhea, prolonged or severe, resulting in severe dehydration (loss of fluid in combination with use of potassium supplements may cause renal toxicity, which may increase risk of hyperkalemia; if potassium supplements are given in presence of diarrhea, serum potassium levels should be monitored); esophageal compression or gastric emptying, delayed or intestinal obstruction or stricture, or peptic ulcer (delayed passage of potassium supplements through the gastrointestinal tract may cause or worsen gastrointestinal irritation, especially with solid dosage forms); renal impairment; cardiac disease


Sodium bicarbonate (Neut)

Sodium bicarbonate is effective but is associated with a sodium load, which may not be desired in patients with associated medical conditions such as hypertension and cardiac failure. In addition, sodium has the adverse effect of promoting cystine excretion.

Adult

4 g PO initially, then 1-2 g q4h

Pediatric

1-10 mEq (23-230 mg)/kg/d PO; adjust dose prn

Anticholinergics or other medications with anticholinergic action (concurrent use with sodium bicarbonate may decrease absorption, reducing effectiveness of the anticholinergic); ciprofloxacin, norfloxacin, or ofloxacin (alkalinization of urine may reduce solubility of ciprofloxacin, norfloxacin, or ofloxacin in urine; patients should be observed for signs of crystalluria and nephrotoxicity); lithium (sodium bicarbonate enhances lithium excretion, possibly resulting in decreased efficacy; this may be partly due to sodium content)

Alkalosis, metabolic or respiratory (may be exacerbated); chloride loss due to vomiting or continuous gastrointestinal suction (increased risk of severe alkalosis); hypocalcemia (increased risk of alkalosis producing tetany)

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

pH determinations, urinary (monitoring is recommended for dosage adjustment when sodium bicarbonate is used as a urinary alkalizer) and renal function determinations (recommended at periodic intervals with long-term use of frequent, repeated dosage); adverse effects include swelling of feet or lower legs, increased thirst, and stomach cramps

Chelating agents


D-penicillamine (Distamine, Cuprimine, Depen)

Penicillamine combines chemically with cystine (cysteine–cysteine disulfide) to form penicillamine–cysteine disulfide, which is more soluble than cystine and is readily excreted. As a result, urinary cystine concentrations are lowered and the formation of cystine calculi is prevented. With prolonged treatment, existing cystine calculi may be gradually dissolved.

Adult

500 mg PO qid
Dissolution of cystine stones: 1-3 g PO qd in divided doses 30 min ac
Prevention of cystine stones: 500 mg-1 g PO qd; some patients may require as much as 4 g qd; maintain urinary level of <300 mg/L

Pediatric

Dose is based on body weight; at first, 7.5 mg/kg (3.5 mg/lb) PO; no dose range established, but urinary cystine levels must be kept <200 mg/L; administer minimum dose required to achieve this level

Antacids, iron, and zinc associated with reduced absorption

Documented hypersensitivity; penicillamine-related agranulocytosis or aplastic anemia; lupus erythematosus

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include allergic reactions (fever, joint pain, skin rash, hives, and/or itching, swelling of lymph glands), fever, pemphigus foliaceus or vulgaris (lesions on the face, neck, scalp, and/or trunk), and stomatitis (ulcers, sores, or white spots on lips or in mouth)
Less frequent adverse effects include agranulocytosis (sore throat and fever with or without chills, sores, ulcers, or white spots on lips or in mouth), aplastic anemia (dyspnea, troubled breathing, tightness in chest, and/or wheezing, sores, ulcers, or white spots on lips or in mouth, swollen and/or painful glands, unusual bleeding or bruising, unusual tiredness or weakness), and glomerulopathy (bloody or cloudy urine; swelling of face, feet, or lower legs; weight gain)
Glomerulopathy may progress to nephrotic syndrome, hemolytic anemia (troubled breathing, exertional, unusual tiredness or weakness), leukopenia (usually asymptomatic, fever or chills, cough or hoarseness, lower back or side pain, painful or difficult urination) or, rarely, thrombocytopenia (usually asymptomatic; rarely, unusual bleeding or bruising; black, tarry stools; blood in urine or stools; pinpoint red spots on skin)
Penicillamine may cause anemia or peripheral neuritis by acting as a pyridoxine antagonist or increasing renal excretion of pyridoxine; requirements for pyridoxine may be increased during penicillamine therapy
Patient monitoring includes blood cell counts, (WBCs and differential), hemoglobin determinations, platelet counts, and direct urinalyses (especially for protein and cells); recommended at least every 2 wk during the first 6 mo of therapy, then monthly thereafter during therapy; however, more frequent testing of blood cell count and urinalyses may be advisable during the first 6 wk of therapy and for several weeks following an increase in maintenance dosage

Reducing agents

These are active reducing agents that undergo thiol-disulfide exchange with cystine (cysteine-cysteine disulfide) to form tiopronin-cystine disulfide, which is more water-soluble than cystine and is readily excreted. As a result, urinary cystine calculi are prevented.


Alpha-mercaptopropionylglycine

An active reducing agent that undergoes thiol-disulfide exchange with cystine. Twenty-five percent of the orally administered dose appears in urine to participate in thiol-disulfide exchange with cystine, thereby reducing renal excretion of sparingly soluble cystine.

Adult

250 mg/d PO; increase up to 1-2 g/d according to cystine excretion

Pediatric

10-15 mg/kg/d PO

Bone marrow depressants and hepatotoxic and nephrotoxic drugs may interact with this medication

Documented hypersensitivity, agranulocytosis, aplastic anemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Gastritis, dermatosis, nephritic syndrome

ACE inhibitors

These are agents that can compete with the disulfide bond in cystine and result in the formation of a cystine complex.


Captopril (Capoten)

Mechanism of action is similar to that of thiols. Contains a free sulfhydryl group that can compete with the disulfide bond in cystine and result in formation of a cystine-captopril complex that is 200 times more soluble than cystine. Has been studied for treatment of cystinuria; however, data are insufficient to establish efficacy and further studies, especially randomized controlled studies, are warranted. May be useful in hypertensive patients with cystinuria who require antihypertensive medications or in patients in whom standard treatment for cystinuria fails.
Rapidly and at least 75% absorbed from gastrointestinal tract. Absorption is reduced by 30-55% in the presence of food. Protein binding is low (25%-30%), primarily because of albumin; biotransformation is hepatic. Onset of action is 15-60 min, and duration of action is approximately 6-12 h and dose-related. Elimination is renal (>95%; 40-50% unchanged; may be less in patients with congestive heart failure), remainder as metabolites.

Adult

75-150 mg/d PO

Pediatric

Appropriate studies on ACE inhibitors in cystinuria have not been performed in pediatric population

Potassium-sparing diuretics may lead to significant increase in serum potassium level; lithium causes reversible increase in serum lithium concentration; allopurinol causes increased risk of leukopenia; antidiabetics can potentiate blood-reducing effects

Documented hypersensitivity; hereditary/idiopathic angioneurotic edema

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Adverse effects include hypotension, skin rash (with or without itching, fever, or joint pain), angioedema, chest pain, hyperkalemia, neutropenia or agranulocytosis, and pancreatitis; monitor blood pressure, leukocyte counts (total and differential), potassium, serum, renal function, and urinary protein (by means of dipstick on first morning urine)

More on Cystinuria

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Treatment & Medication: Cystinuria
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Multimedia: Cystinuria
References
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Further Reading

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Keywords

cystinuria, urolithiasis, cystine urolithiasis, urinary calculi, stone formation, amino acids, cystine, cysteine, SLC3A1, SLC7A9, rBAT, urinary alkalinization, hydration, D-penicillamine, tiopronin, Thiola, captopril, extracorporeal shockwave lithotripsy, ESWL, extracorporeal shock wave lithotripsy, retrograde endoscopic lithotripsy, percutaneous nephrolithotomy, PCNL, stone removal, urinary tract stone, kidney stone, recurrent stone formation, stone recurrence, urinary calculus, cystic oxide, cystine stones, cystine stone formers, ornithine, arginine, lysine

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Contributor Information and Disclosures

Author

Chandra Shekhar Biyani, MBBS, MS, DUrol, FRCS(Urol), FEBU, Consulting Urologist, Department of Urology, Pinderfields General Hospital, UK
Chandra Shekhar Biyani, MBBS, MS, DUrol, FRCS(Urol), FEBU is a member of the following medical societies: British Association of Urological Surgeons, British Medical Association, European Association of Urology, and International College of Surgeons
Disclosure: Nothing to disclose.

Coauthor(s)

Jon Cartledge, MD, FRCS (Urol), Consulting Urologist, Pyrah Department of Urology, St James's University Hospital, UK
Jon Cartledge, MD, FRCS (Urol) is a member of the following medical societies: British Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Bradley Fields Schwartz, DO, FACS, Professor of Urology, Director, Center for Laparoscopy and Endourology, Department of Surgery, Southern Illinois University School of Medicine
Bradley Fields Schwartz, DO, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Association of Military Osteopathic Physicians and Surgeons, Endourological Society, Society of Laparoendoscopic Surgeons, and Society of University Urologists
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Direct of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

J Stuart Wolf Jr, MD, FACS, David A Bloom Professor of Urology, Director of Division of Minimally Invasive Urology, Department of Urology, University of Michigan
J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of Urologic Oncology
Disclosure: Terumo Corporation Consulting fee Consulting; Omeros Corporation Consulting fee Consulting

Chief Editor

Bradley Fields Schwartz, DO, FACS, Professor of Urology, Director, Center for Laparoscopy and Endourology, Department of Surgery, Southern Illinois University School of Medicine
Bradley Fields Schwartz, DO, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Association of Military Osteopathic Physicians and Surgeons, Endourological Society, Society of Laparoendoscopic Surgeons, and Society of University Urologists
Disclosure: Nothing to disclose.

 
 
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