Urolithiasis, kidney stones, renal stones, and renal calculi are interchangeably used to refer to the accretion of hard, solid, nonmetallic minerals in the urinary tract (see the image below). Nephrocalcinosis is a term that refers to increased calcium content in the parenchyma of the kidney.
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Three groups of kidney stones are shown. Groups at left and center contain varying concentrations of calcium, phosphate, and oxalate. The group of sto....
Patient and parent education regarding risk factors for additional stone formation and diet and medication complications is very important. For patient education information, see the Kidneys and Urinary System Center, as well as Kidney Stones and Blood in the Urine.
For more information, see the Medscape Reference topic Nephrolithiasis.
Renal, urologic, endocrine, and metabolic disorders may lead to the development of crystallized material in the urinary system. Stones are most often classified into groups based on their chemical components.
Materials that produce stones in the urinary tract of children include the following:
Calcium with phosphate or oxalate
Purine derivatives
Magnesium ammonium phosphate (struvite)
Cysteine
Combinations of the preceding items
Drugs or their metabolites (eg, phenytoin, triamterene)
Melamine-contaminated milk powder consumption
In fluids contained within the urinary system, interaction between factors that promote and factors that inhibit crystallization is continuous. When solutes in solution are at concentrations below their solubility product (subsaturation of stone-forming compounds in the urine), added crystals dissolve (undersaturated region). Spontaneous precipitation can occur when concentration of constituents is above the formation product. The metastable region lies between solubility product and formation product. Existing crystals can grow, but spontaneous precipitation does not occur.
Renal stones occur as a result of the following 3 factors:
Supersaturation of stone-forming compounds in urine
Presence of chemical or physical stimuli in urine that promote stone formation
Inadequate amount of compounds in urine that inhibit stone formation (eg, magnesium, citrate)
Contributing factors
Numerous dietary items may contribute to renal stone production. A high oxalate intake may contribute to calcium oxalate stone production. Excessive purine intake may contribute to the production of stones containing uric acid and uric acid plus calcium components. A ketogenic diet, prescribed to reduce seizures, places children at risk for both uric acid and calcium stone formation.
In general, urinary calcium increases with dietary calcium intake (see Hypercalciuria). Urinary calcium increases in patients with high sodium chloride intake. Dietary phosphate restriction, if severe, increases urine calcium excretion. A diet high in protein from animal sources, glucose or sucrose increases urinary calcium and, in some cases, may contribute to stone formation.[1] Vitamins A and D can contribute to calcium urolithiasis when taken in excessive amounts. Fructose consumption is also associated with an increased risk of kidney stones.[2]
Drug intake may contribute to stone formation in 3 basic ways (see the table below).
Table 1. Stone Formation
View Table
See Table
First, the drug or its metabolites may precipitate as stones (eg, phenytoin, triamterene, sulfadiazine, felbamate, ceftriaxone[3] ).
Second, the drug may increase the concentration of stone-forming minerals by increasing the filtered load or decreasing the tubular reabsorption. For example, anticancer agents increase the filtered load of uric acid and glucocorticoids increase the filtered load of calcium. Allopurinol increases the filtered load of xanthine in patients with tumor lysis to produce xanthinuria. Furosemide decreases tubular calcium reabsorption, leading to increased urine calcium concentration.
Third, the drug may alter urine pH, decreasing the solubility of a stone-forming agent. In children with distal renal tubular acidosis, bicarbonate probably contributes to stone formation by further alkalinizing the urine.
Fluid intake is important quantitatively and qualitatively. A low fluid intake leads to concentrated urine and increases the risk of stone formation. Water may have a high mineral content in some areas. Milk contains significant calcium and vitamin D. Orange juice may be supplemented with calcium. Tea contains oxalate and often sucrose. Many drinks (eg, sports drinks) contain sodium chloride and sucrose.
Some diseases, or the medications used to treat them, increase stone formation risk. Examples include distal renal tubular acidosis, short-gut syndrome, inflammatory bowel disease, intractable seizures, and cystic fibrosis. Urolithiasis is not uncommon in pediatric patients who have undergone a kidney transplant.[4] Factors associated with post-kidney transplant urolithiasis include retention of suture material, recurrent urinary tract infection, hypercalciuria, and urinary stasis. Gastrostomy tube–fed children are at higher risk of urolithiasis that may be related to concomitant topiramate administration, urinary tract infection, and shorter G-tube duration possibly affecting subclinical chronic dehydration.[5]
A population-based, case–control study by Tasian et al that included 25,981 patients with nephrolithiasis reported that oral antibiotics were associated with increased odds of nephrolithiasis. The adjusted odds ratio (95% confidence interval) was 2.33 (2.19 to 2.48) for sulfas, 1.88 (1.75 to 2.01) for cephalosporins, 1.67 (1.54 to 1.81) for fluoroquinolones, 1.70 (1.55 to 1.88) for nitrofurantoin/methenamine, and 1.27 (1.18 to 1.36) for broad-spectrum penicillins. The study also reported that the greatest odds for nephrolithiasis were recent exposure and exposure at younger age.[6]
Risk factors
Risk factors for pediatric urolithiasis include the following:
Habitually low urine volume
High urine excretion of calcium
High urine excretion of uric acid
High urine excretion of oxalate
Low urine pH: Uric acid and cysteine are less soluble in acid urine.
High urine pH: Struvite and calcium phosphate are less soluble in alkaline urine.
Nidus for crystal precipitation: A nidus for crystal precipitation (eg, uroepithelial surface properties that affect crystal retention) occurs when the crystalline lattice structure of one crystal is similar to another crystal and the second crystal grows on the first.
In children, hypercalciuria and a reduction in the gap between calcium phosphate upper limit of metastability and supersaturation are significant risk factors for stones.[7] Other factors such as developmental abnormalities of the urinary tract, urinary obstruction, urinary stasis, and infection with urea-splitting microorganisms may also be important.
Frequency of urolithiasis in children has not been studied in a systematic population-based fashion. Institutional and case reports indicate regional variation. A significant increase in the number of children diagnosed with and treated for urolithiasis has occurred in the last decade.[8]
United States statistics
Children with stones now account for 1 in 685 pediatric hospitalizations in the United States. Surprisingly, more than half the patients are younger than 13 years at hospitalization.[9] Urolithiasis is relatively uncommon in the United States compared with some other areas of the world, possibly because of diet or public health measures. Endemic bladder stones (uric acid and ammonium acid urate) are rare in the United States, though common in developing countries.
The southeast region of the United States has a higher frequency of kidney stone formation in adults than do other regions of the United States. The reason for a higher incidence of stone formation in the southern United States is unknown. Suggested factors include climate, diet, genetics, state of hydration, and bacterial colonization.
A study by Tasian et al examined trends in the annual incidence and cumulative risk of nephrolithiasis among children and adults living in South Carolina over a 16-year period. The study reported that the incidence of kidney stones has increased among young patients (26% increase in 5 years for those 15-19 years of age). Incidence also increased 15% per 5 years among females and 15% per 5 years among African Americans.[10]
Urinary tract stones in children are a relatively infrequent problem. Regional rates of stone formation in children have not been reported.
International statistics
Stones are more common in certain areas. In Europe, kidney stones occur in 1-2 children per million population per year. In underdeveloped countries, children more frequently have endemic bladder stones than renal stones. Endemic bladder calculi are common in developing countries where dietary protein is mostly derived from plant sources rather than meat. These areas include Eastern Europe, Southeast Asia, India, and the Middle East. Upper urinary calculi associated with urease-producing bacterial infection occur in England and Europe.
A study by Pong et al, that investigated the incidence for pediatric urolithiasis in Taiwan from 1998-2007, reported that the trend of annual newly diagnosed incidences for boys, girls, and all children declined. This also coincided with a decline in medical costs and annual medical care visits for pediatric urolithiasis during this period.[11]
Age-, sex-, and race-related demographics
Peak presentation for adults is middle age. Adults are most often afflicted with calcium oxalate or calcium phosphate stones. In some cases, the primary cause of stone formation cannot be identified.
Children can present with stones at any age (eg, premature newborn to teenager). In children, calcium stones are most common. The approximate frequency of kidney stone types in the pediatric age group is calcium with phosphate or oxalate (57%), struvite (24%), uric acid (8%), cystine (6%), endemic (2%), mixed (2%), and other types (1%). With children, particularly younger children, the primary cause of stone formation (eg, hypercalciuria, hyperuricosuria) can usually be identified with a through evaluation.
Although stones are more frequent in men than in women (4:1), the boy-to-girl ratio (3:2) is closer to equal.
No population-based studies have been performed, but institutional reports indicate that, in the United States, white children develop urolithiasis more frequently than children who are black, Asian American, or Latin American.
Generally, the prognosis for children with kidney stones is good; most children do well. However, mortality and significant morbidity sometimes occur. Urolithiasis during childhood can have important lifelong implications for some patients.
Kidney stones are not usually fatal, although some primary conditions that produce kidney stones (eg, Lesch-Nyhan syndrome, oxalosis) can lead to death from problems associated with the primary disease or complications of renal failure. Infected stones may lead to urosepsis and death. Complete untreated renal outflow obstruction causes renal failure.
Acute renal colic may be very painful. Infected stones may produce pain as well as sepsis. Children who develop frequent painful stones or stones that require painful treatment such as urologic stone removal or extracorporeal shockwave lithotripsy (ESWL) may experience considerable morbidity.
Stones are classified by their composition. Knowledge of composition may help to design preventive therapy, but the chemical composition of a stone usually has little to do with the clinical manifestations. The clinical manifestations are related more to the following 5 factors:
The size of the stone (larger stones tend to be more symptomatic, although some large stones produce few symptoms)
The location of the stone
The production of urinary outflow obstruction
The movement of the stone (eg, from the renal pelvis to bladder)
The presence of infection
Presentation usually depends on age; symptoms such as flank pain and hematuria are more common in older children. Nonspecific symptoms (eg, irritability, vomiting) are common in very young children.
The following are 5 fairly typical presentations of stone disease in children:
Intense pain that suddenly occurs in the back and radiates downward and centrally toward the lower abdomen or groin
Hematuria, usually gross, occurring with or without pain: Hematuria may or may not be present. In a series of adults in whom helical computed tomography (CT) scanning was used to identify lithiasis in the emergency department (ED), one third had 5 or fewer red blood cells (RBCs) per high-powered field.[12] No similar study has been performed in children, but many pediatric nephrologists have identified stone disease children with symptoms, stones, and no hematuria.
Infection leading to radiologic imaging in which a stone is identified
Asymptomatic stones, which are sometimes identified when abdominal imaging is performed for another reason
Persistent microscopic hematuria, which consists of 5 or more RBCs per high-power field in 3 of 3 consecutive centrifuged urine specimens obtained at least 1 week apart
History should include questions to identify frequent urinary tract infections, frequent bouts of abdominal pain, hematuria (gross or microscopic), passage of previous calculus, dietary intake (eg, oxalate, purine, calcium, phosphate, fructose, animal protein), drug intake (eg, anticancer drugs, glucocorticoids, allopurinol, loop diuretics), vitamin intake (A, D), fluid intake, habitual fluid type (eg, water, milk, tea, sports drinks),
The history should also include questions on chronic disease (eg, renal tubular acidosis, inflammatory bowel disease, short-gut syndrome, intractable seizures, cystic fibrosis), prior urologic surgery (eg, kidney transplant), or recent immobilization.
Because some renal stone diseases may be inherited, a careful family history to identify other family members with stones is important. In some reports, as many as 70% of children with idiopathic hypercalciuria (see Hypercalciuria) have a family history of stones. The cause of idiopathic hypercalciuria is unknown, but it may be transmitted as an autosomal dominant trait.
Other inherited conditions to be considered include cystinuria, an autosomal recessive defect of amino acid transport that leads to cystine kidney stones, glycinuria, a rare inherited renal tubular defect producing oxalate stones; xanthinuria, an autosomal recessive disorder that produces xanthine urolithiasis; and primary hyperoxaluria, produced by an autosomal disorder leading to oxalate stones. Several inherited disorders in purine metabolism lead to uric acid stones (Lesch-Nyhan disease is probably the best known).
The physical examination in children with urolithiasis is influenced by several factors. The most important include age, pain, infection, and the underlying process producing the stone.
For example, an infant with pain may have inconsolable crying; a teenager may have obvious costovertebral angle tenderness. Manifestations of infection may range from no physical abnormalities to fever to a physical picture consistent with urosepsis (eg, fever, tachycardia, hypotension, cold clammy skin). Conditions such as Lesch-Nyhan disease, inflammatory bowel disease (IBD), and cystic fibrosis have findings specific for the disease.
A routine physical examination should be performed, including the following anthropometric data:
Height
Weight
Muscle mass
Systemic diseases associated with stones, including the following, may produce decreased growth:
Distal renal tubular acidosis
Oxalosis
IBD
Cystic fibrosis
Short-gut syndrome
Many children with kidney stones have normal physical examination findings. Exceptions to normal findings on physical examination include the following:
Hypertension (may be present with urinary obstruction or pain)
Tachycardia in children with pain
Costovertebral angle tenderness
Oxalosis (flecked retina)
Adolescents with primary hyperparathyroidism in whom stones are the presenting feature (eg, hypertension associated with hypercalcemia)
Rickets, stones as part of Dent disease
Complications
The primary complications of urolithiasis include obstruction of the urinary tract, renal parenchymal damage, infection, and adverse effects of medication or diet.
In children, laboratory studies only provide suggestive evidence of a kidney stone; however, certain laboratory studies (eg, calcium or uric acid excretion) may be very helpful in identifying risk factors for additional stone formation. Imaging studies are valuable. Direct assessment of stones is vital.
In children with identified or strongly suspected stone disease, obtain the following laboratory studies:
Complete blood count (CBC)
Electrolyte, blood urea nitrogen (BUN), creatinine, calcium, phosphorus, alkaline phosphatase, uric acid, total protein, albumin, parathyroid hormone (PTH), and vitamin D metabolite levels
Spot urinalysis and culture, including ratio of calcium, uric acid, oxalate, cystine, citrate, and magnesium to creatinine
Urine tests, including a 24-hour urine collection for calcium, phosphorus, magnesium, oxalate, uric acid citrate, cystine, protein, and creatinine clearance
Renal ultrasonography is very effective for identifying stones in the urinary tract. Generally, ultrasonography should be used as a first study. If no stone is found but symptoms persist, helical (spiral) computed tomography (CT) scanning is indicated. Noncontrast spiral CT scanning is the most sensitive test for identifying stones in the urinary system. It is safe, rapid, and has been shown to have 97% sensitivity and 96% specificity.
Many radiopaque stones can be identified with a simple abdominal flat-plate examination. Intravenous pyelography is rarely used in children.
Go to Imaging Urinary Calculi for complete information on this topic.
For hypercalcinuria, hypercystinuria, or hyperoxaluria, please refer to Hypercalciuria and Hyperoxaluria for further evaluation.
Attempting to obtain a stone for histologic and crystallographic evaluation is essential. It is usually obtained by straining urine in older children or examining diapers in young children (see image below). The content of the stone (ie, cysteine versus calcium versus uric acid) may be the most important element in developing a treatment program to prevent further stone formation (see the image below).
View Image
Three groups of kidney stones are shown. Groups at left and center contain varying concentrations of calcium, phosphate, and oxalate. The group of sto....
Medical care largely depends on the type of presentation. Care may range from observation to emergency treatment. An obstructed infected portion of the urinary tract is a surgical emergency. (See Surgical Care, below.)
A child presenting with acute colic and gross hematuria can be managed with analgesics. Narcotics may be required, as well as enteral or parenteral hydration. When a stone is small and at the ureteropelvic or ureterovesical junction, it may pass spontaneously; a few days of observation for spontaneous passage may be indicated prior to more aggressive intervention.
A stone that completely obstructs the bladder outlet should be treated with catheterization using a Foley catheter. Once urine outflow has been established, the approach for removal vesicostomy versus cystoscopy versus lithotripsy is usually determined by the pediatric urologist. (See Surgical Care, below.)
Children with asymptomatic stones detected while screening for another problem should have blood and urine testing performed to identify underlying metabolic abnormalities.
Immobility may contribute to stone formation in some children. Generally, children with diseases and injuries should be mobilized as soon as possible. No activity restriction is necessary in urolithiasis.
The specific aims of surgical care include drainage of the urinary tract, removal of stones present in the urinary tract, and surgical correction of anatomic abnormalities, which may promote additional stone formation.
A child with an acute presentation indicative of an infected stone should be referred immediately to a pediatric urologist for drainage, antibiotic treatment, and supportive care.
Stones may need to be removed by a pediatric urologist. The removal technique used usually depends on the stone size and location. Surgical treatments may include ureteroscopic stone extraction,[13] percutaneous nephrolithotomy, open stone surgery, and/or extracorporeal shockwave lithotripsy (ESWL). Alpha-1 adrenergic blocker agents, such as doxazosin, have been used as medical expulsive treatment in children with distal uretral stones.[14, 15]
The overall role of diet is to supply adequate quantities of material for growth and metabolism without a surplus of relatively insoluble material that requires urinary excretion. Most materials (eg, calcium, phosphate, oxylate, uric acid, cysteine) enter body fluids, and thus the urine, from one of the following 3 sources: dietary intake, de novo metabolic production, or normal turnover.
For example, calcium and phosphate are derived from dietary intake and normal turnover with bone remodeling. Oxalate is abundant in nature and enters body fluid via dietary intake and as an end product of de novo metabolism. Small quantities of uric acid are in the diet, but most uric acid is produced as an end product of purine metabolism. Purine largely comes from dietary intake. Cysteine is produced from dietary intake, normal metabolic cysteine turnover, and de novo production from methionine.
Dietary considerations depend on the type of stone. A high fluid intake leading to increased urine output is safe and generally beneficial for children with all types of stones, but stone analysis to identify the minerals present is critically important.
No randomized, prospective, double-blind studies describing the outcomes of groups of children with different metabolic stone-forming diseases that are controlled for diet alone are available. Because stone disease can cause considerable morbidity in some children, clinical trials may develop in the future.
Children with stones composed of calcium and who have excessive calcium intake or idiopathic gastrointestinal absorptive hypercalciuria may benefit from lowered dietary calcium intake. The author first restricts the calcium intake to the recommended daily allowance (RDA). The RDA was developed by estimating the daily need and then doubling. A dietitian is important in helping to develop this type of specialized diet. The goal is to lower urinary calcium such that no new stones are formed without producing calcium deficiency.
In some cases, diets containing calcium levels lower than the RDA may be required. If a diet with less than the RDA of calcium is considered, the parents and child should be included in discussion of risks versus benefits (ie, potential calcium deficiency versus decreased stone production).
In children with hypercalcinuria, restrict sodium to RDA for age. In an adult study in 2002, Borghi et al reported that sodium and animal protein restriction were more effective in reducing calcium stone formation than calcium restriction.[1] To restrict children to the RDA for sodium and animal protein is probably not harmful and may be helpful with respect to stone formation.
Children with hyperuricosuria may benefit from avoiding purine-rich foods. Lowering purine intake to the RDA may lower serum uric acid and urinary uric acid excretion to the reference range. In the past, children receiving pancreatic enzymes ingested extra purine, which contributed to increased uric acid excretion. With newer enzyme preparations, excessive purine intake is no longer the case. In children with inborn errors of purine metabolism, lowering purine intake alone does not normalize urinary uric acid excretion.
Use caution; reduction of dietary components is intended to reduce urinary excretion, but be cautious not to develop a diet so restrictive that it produces nutritional deficiency.
Consultation with a pediatric dietitian, a pediatric nephrologist, and a pediatric urologist is usually appropriate. Generally, a pediatric nephrologist is most experienced with evaluation and management of renal stone disease in children. Consult a pediatric urologist for children who might need shock wave lithotripsy, percutaneous nephrolithotomy, ureteroscopy, or open surgery.
The primary goals of inpatient care are to treat life-threatening infection, surgically remove stones, rehydrate a child with vomiting and dehydration, and manage severe pain. In the author’s experience, many children with kidney stones do not require inpatient care.
Effects of treatment should be monitored by measurement of urinary and plasma chemistries 1 month after initiating treatment and then every 2 months until a steady state is established. The blood and urine analytes measured depend on the type of stone, diet restrictions, and medication prescribed (vide infra).
Because of increased incidence of low bone density in children with hypercalciuria and nephrolithiasis, dual emission x-ray absorptiometry (DEXA) scanning should be performed at onset and then yearly in children aged 5 years and older. The test provides an absolute density measurement that can be monitored over time.[16]
Patients should undergo annual imaging with renal ultrasonography to look for new or growing stones. New stone formation or growth in size suggests that therapy is ineffective and should be reevaluated.
Children with recurrent calculi who are on restrictive diets (eg, restricting calcium, purine derivatives) or medications that affect the excretion of these items should have their therapy assessed initially and reassessed periodically to determine in each case that treatment is beneficial and that the benefits outweigh the risks. Children on calcium restriction should have serum calcium, parathyroid hormone (PTH), and urine calcium excretion determined at onset, in 2 months, and then at 6-month intervals.
Children receiving thiazides should have serum electrolytes, cholesterol, uric acid, and urinary calcium excretion measured at onset, at 2 months, and then at 6-month intervals. Children receiving allopurinol should have a complete blood count (CBC), liver function tests, and urinary uric acid excretion tests performed every 2 months.
The medications listed above are used for both inpatient and outpatient care. Prevention of new stone formation requires a combination of medication, large fluid intake, and diet restriction described above.
A study by Saitz et al compared 24-hour urine profiles in children with only one stone incident to those with recurrent stone incidents. The study reported that higher values of super-saturation calcium oxalate was associated with recurrent stone disease and that lower urinary volume may also be associated with recurrent episodes. Further investigation is needed.[17]
Medical therapy depends on the type of stone produced. Children with idiopathic hypercalciuria caused by renal tubular calcium leak may benefit from treatment with a thiazide. If idiopathic hypercalcinuria is gastrointestinal (GI) absorptive and a low-calcium diet does not return urinary calcium levels to the reference range, neutral sodium phosphate may be beneficial in reducing dietary calcium absorption. Chelating agents such as cellulose sodium phosphate (Calcibind) are no longer available on the US market.
Hypocitraturia is treated with oral potassium citrate. Supplemental citrate leads to correction of hypocitraturia.
Struvite stones require treatment with an appropriate antibiotic. Surgical intervention or ESWL may be necessary if the stone produces high-grade obstruction, if antibiotic therapy is not adequately eliminating infection, or after infection is cleared to remove stone fragments.
Uric acid stones require alkalinization of urine with sodium bicarbonate or potassium citrate in 4 divided doses. Urine pH levels should be maintained at 7.5 or greater. Uric acid is much more soluble in alkaline than acid urine. Allopurinol is indicated in children with uric acid lithiasis whose daily uric acid excretion exceeds the reference range.
The medical management of cystinuria is mainly based on hyperhydration and urine alkalinization. Sulfhydryl agents such as tiopronin should be added.
Clinical Context:
Sodium citrate and citric acid mixture is indicated for systemic metabolic acidosis (ie, renal tubular acidosis), urinary alkalinization, or hypocitraturia. It contains disodium citrate. It is administered orally and is metabolized to bicarbonate by the liver. The preparation contains 500 mg sodium citrate and 334 mg citric acid per 5 mL (ie, 1 mEq potassium and 1 mEq sodium per 1 mL).
Sodium citrate and potassium citrate mixture (Citra-3, Tricitrates)
Clinical Context:
Sodium citrate and potassium citrate mixture is indicated for treatment of systemic metabolic acidosis, urinary alkalinization, or hypocitraturia. It is administered orally and metabolized to bicarbonate in the liver. Each 5 mL of the preparation contains sodium citrate 500 mg, citric acid 334 mg, and potassium citrate 550 mg (each mL contains 1 mEq potassium, 1 mEq sodium, and 2 mEq bicarbonate).
Alkalinizing agents are used to increase urinary pH and/or provide increased citrate in the urine in persons with hypocitruria. Both have a tendency to increase solubility of some minerals.
Clinical Context:
Hydrochlorothiazide, by an unknown mechanism, decreases urinary calcium excretion. By lowering urinary calcium concentration, the risk of calcium forming complexes with anions (eg, oxalate, phosphate) is reduced.
Clinical Context:
Allopurinol decreases uric acid production. Administer before meals and with extra fluid orally. Maintain urine output at approximately 1.5 mL/kg/h with oral fluid unless this is contraindicated.
A xanthine oxidase inhibitor is used to lower urinary uric acid. The doses provided in the table are for children with uric acid or calcium-urate renal calculi. Physicians treating gout, hyperuricemia, or uric acid nephropathy should consult other articles.
Sahar Fathallah-Shaykh, MD, Associate Professor of Pediatric Nephrology, University of Alabama at Birmingham School of Medicine; Consulting Staff, Division of Pediatric Nephrology, Medical Director of Pediatric Dialysis Unit, Children's of Alabama
Disclosure: Nothing to disclose.
Coauthor(s)
Richard Neiberger, MD, PhD, Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital
Disclosure: Nothing to disclose.
Specialty Editors
Mary L Windle, PharmD, Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Luther Travis, MD, Professor Emeritus, Departments of Pediatrics, Nephrology and Diabetes, University of Texas Medical Branch School of Medicine
Disclosure: Nothing to disclose.
Chief Editor
Craig B Langman, MD, The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago
Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Horizon Pharmaceuticals); ; Dicerna, Jannsen Pharmaceuticals.
Additional Contributors
Deogracias Pena, MD, Medical Director of Dialysis, Medical Director of Pediatric Nephrology and Transplantation, Cook Children's Medical Center; Clinical Associate Professor, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Medical Director of Pediatric Nephrology, Florida Hospital for Children
Saitz TR, Mongoue-Tchokote S, Sharadin C, et al. 24 hour urine metabolic differences between solitary and recurrent stone formers: results of the Collaboration on Urolithiasis in Pediatrics (CUP) working group. Journal of Pediatric Urology. April 20, 2017.
Three groups of kidney stones are shown. Groups at left and center contain varying concentrations of calcium, phosphate, and oxalate. The group of stones on the right is composed of cysteine.
Three groups of kidney stones are shown. Groups at left and center contain varying concentrations of calcium, phosphate, and oxalate. The group of stones on the right is composed of cysteine.
Three groups of kidney stones are shown. Groups at left and center contain varying concentrations of calcium, phosphate, and oxalate. The group of stones on the right is composed of cysteine.
Mechanism of Stone Formation
Drug
Primary Stone Composition
Crystallization of highly excreted, poorly soluble drug or metabolite causes stone formation.
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