AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

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. Nephrocalcinosis is a term that refers to increased calcium content in the parenchyma of the kidney.

Pathophysiology

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 (1) calcium with phosphate or oxalate, (2) purine derivatives, (3) magnesium ammonium phosphate (struvite), (4) cysteine, (5) combinations of the preceding items, and (6) drugs or their metabolites (eg, phenytoin, triamterene).

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.

Frequency

United States

Frequency of urolithiasis in children has not been studied in a systematic population-based fashion. Institutional and case reports indicate regional variation. In the United States, the incidence of urolithiasis varies between 1 case per 1000 and 1 case per 7600 hospital admissions. 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 common in the developing countries but are rare in the United States. Endemic bladder stones are frequent in areas where dietary protein is mostly derived from cereal grains rather than meat. 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. Regional rates of stone formation in children have not been reported.

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. Urinary tract stones in children are a relatively infrequent problem.

International

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 derived from plant sources. 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.

Mortality/Morbidity

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. When urolithiasis occurs during childhood it has important lifelong implications.

Acute renal colic may be very painful. Infected stones may produce pain, sepsis, or both. 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.

Race

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.

Sex

Stones are more frequent in men than in women (4:1), although the boy-to-girl ratio (3:2) is closer to equal.

Age

Peak presentation for adults is middle age. Children can present with stones at any age (eg, premature newborn to teenager). Adults are most often afflicted with calcium oxalate or calcium phosphate stones. In some cases, the primary cause of stone formation cannot be identified. 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.

CLINICAL

Section 3 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
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• Follow-up
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History

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 more related to (1) the size of the stone (larger stones tend to be more symptomatic, although some large stones produce few symptoms), (2) the location of the stone, (3) the production of urinary outflow obstruction, (4) the movement of the stone (eg, from the renal pelvis to bladder), and (5) 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 CT scanning was used to identify lithiasis in the emergency department, one third had 5 or fewer RBCs per high-powered field.¹ 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
• Some renal stone diseases may be inherited. 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. Cystinuria is an autosomal recessive defect of amino acid transport that leads to cystine kidney stones. Glycinuria is a rare inherited renal tubular defect producing oxylate stones. Xanthinuria is an autosomal recessive disorder that produces xanthine urolithiasis. Primary hyperoxaluria is produced by an autosomal disorder leading to oxylate stones. Several inherited disorders in purine metabolism lead to uric acid stones (Lesch-Nyhan disease is probably the best known); therefore, a careful family history to identify other family members with stones is important.
• 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, drug intake, vitamin intake, fluid intake, habitual fluid type, chronic disease (eg, renal tubular acidosis or short-gut syndrome), prior urologic surgery, or recent immobilization (vide infra).
• • 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.² Fructose consumption is also associated with an increased risk of kidney stones.³
  • Drug intake may contribute to stone formation in 3 basic ways. First, the drug or its metabolites may precipitate as stones (eg, phenytoin, triamterene, sulfadiazine, felbamate, ceftriaxone⁴). 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.
    
    Stone Formation
    

    Mechanism of Stone Formation	Drug	Primary Stone Composition
    Crystallization of highly excreted, poorly soluble drug or metabolite causes stone formation.	Phenytoin, triamterene, sulfonamides, felbamate, ceftriaxone, indinavir, ciprofloxacin, guaifenesin/ephedrine	Drug or its metabolites
    Drug may increase the concentration of stone-forming minerals.	1. Anti-cancer drugs 2. Glucocorticoid 3. Allopurinol (if used in tumor lysis) 4. Loop diuretics 5. Calcium and vitamin D	1. Uric acid 2. Calcium 3. Xanthine 4. Calcium oxalate 5. Calcium
    Drug inhibits activity of carbonic anhydrase enzymes in the kidney, causing metabolic acidosis, hypocitraturia, and elevated urine pH.	Topiramate, zonisamide, acetazolamide	Calcium phosphate

• • Vitamins A and D can contribute to calcium urolithiasis when taken in excessive amounts.
  • 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.
  • Chronic illnesses may be a manifestation of stone disease. Prolonged unexplained fever may reflect an infected staghorn calculus. 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.⁵ Factors associated with post–kidney transplant urolithiasis include retention of suture material, recurrent urinary tract infection, hypercalciuria, and urinary stasis.

Physical

The physical examination in children with urolithiasis is influenced by several factors. The most important include age, pain, infection, and underlying process producing the stone. An infant with pain may have inconsolable crying; a teenager may have obvious costovertebral angle tenderness. 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, and cystic fibrosis have findings specific for the disease.

• A routine physical examination should be performed, including anthropometric data. Many children with kidney stones have normal physical examination findings.
• • Height
  • Weight
  • Muscle mass
• Systemic diseases associated with stones, including the following, may produce decreased growth:
• • Distal renal tubular acidosis
  • Oxalosis
  • Inflammatory bowel disease
  • Cystic fibrosis
  • Short-gut syndrome
• 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

Causes

• 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)
• Additional risk factors 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.
• Factors such as developmental abnormalities of the urinary tract, urinary obstruction, urinary stasis, and infection with urea-splitting microorganisms may also be important.

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Anatomical abnormalities (eg, ureteropelvic junction [UPJ] obstruction)
Drugs
Infection
Loin pain hematuria syndrome
Renal infarction
Renal vein thrombosis
Trauma
Tumors

WORKUP

Section 5 of 11  

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Lab Studies

• In children, laboratory studies only provide suggestive evidence of a kidney stone.
• Laboratory studies (eg, calcium or uric acid excretion) may be very helpful in identifying risk factors for additional stone formation.
• In children with identified or strongly suspected stone disease, obtain the following laboratory studies:
• • CBC count
  • Electrolyte, 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

Imaging Studies

• The most sensitive test for identifying stones in the urinary system is noncontrast helical CT scanning. 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.
• 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, spiral CT scanning is indicated.
• Intravenous pyelography is rarely used in children.

Other Tests

• For hypercalcinuria, hypercystinuria, or hyperoxaluria, please refer to Hypercalciuria and Hyperoxaluria for further evaluation.

Histologic Findings

• 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.
• Content (ie, cysteine versus calcium versus uric acid) of the stone may be the most important element in developing a treatment program to prevent further stone formation.

TREATMENT

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Medical Care

The overall goals of medical care are to (1) prevent additional renal damage, which may lead to loss of renal parenchyma; (2) manage pain associated current stone(s); (3) expedite passage or removal of any stones present; and (4) prevent new stones from forming.

• 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 requiring drainage, antibiotic treatment, and supportive care.
• 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. If the stone is small, it may pass spontaneously.
• 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.
• Children with asymptomatic stones detected while screening for another problem should have blood and urine testing performed to identify underlying metabolic abnormalities.

Surgical Care

The main goals 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 definitive treatment.
• 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, percutaneous nephrolithotomy, open stone surgery, and/or ESWL.

Consultations

• Consultation with a pediatric dietitian, pediatric urologist, and pediatric nephrologist 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.

Diet

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.
• Stone formations in children are infrequent. 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). 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. 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). The RDA was developed by estimating the daily need and then doubling. In some cases, diets containing calcium levels lower than the RDA may be required.
• 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.² 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.

Activity

• 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.

MEDICATION

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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 GI absorptive and a low-calcium diet does not return urinary calcium levels to the reference range, cellulose sodium phosphate or neutral sodium phosphate may be beneficial in reducing dietary calcium absorption.

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.

Drug Category: Alkalinizing agents

These 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.

Drug Category: Diuretics

These agents are used to decrease urinary calcium excretion.

Drug Category: Chelating agents

These agents are used to reduce calcium absorption from lower GI tract.

Drug Category: Xanthine oxidase inhibitors

Allopurinol is used to lower urinary uric acid. The doses below are for children with uric acid or calcium-urate renal calculi. Physicians treating gout, hyperuricemia, or uric acid nephropathy should consult other articles.

FOLLOW-UP

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Further Inpatient Care

• 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.

Further Outpatient Care

• Effects of treatment should be monitored by measurement of urinary and plasma chemistries one 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 stone, diet restrictions, and medication prescribed (vide infra).
• • 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, PTH, and urine calcium excretion determined at onset, in 2 months, and then at 6-month intervals.
• Dual emission x-ray absorptiometry (DEXA) scanning should be performed at onset and then yearly. No normative data for children exist at present. The test provides an absolute density measurement that can be monitored over time.
• 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 CBC count, liver function tests, and urinary uric acid excretion tests performed every 2 months.

In/Out Patient Meds

• The medications listed above are used for both inpatient and outpatient care.

Transfer

• No special requirements are indicated for transfer from one physician or facility to another.

Deterrence/Prevention

• Prevention of new stone formation requires a combination of medication, large fluid intake, and diet restriction described above.

Complications

• The primary complications of urolithiasis include obstruction of urinary tract, renal parenchymal damage, infection, and adverse effects of medication or diet.

Prognosis

• Generally, the prognosis for children with kidney stones is good. Occasionally, death or significant morbidity occurs; however, most children do well.

Patient Education

• Patient and parent education regarding risk factors for additional stone formation and diet and medication complications is very important.
• For excellent patient education resources, visit eMedicine's Kidneys and Urinary System Center. Also, see eMedicine's patient education articles Kidney Stones and Blood in the Urine.

MISCELLANEOUS

Section 9 of 11  

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• Miscellaneous
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Medical/Legal Pitfalls

• The major legal pitfalls are failure to diagnose or misdiagnosis, which lead to fatality, ongoing pain and suffering, or additional significant renal damage.

MULTIMEDIA

Section 10 of 11  

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• Differentials
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  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.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

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• References

1. Bove P, Kaplan D, Dalrymple N, et al. Reexamining the value of hematuria testing in patients with acute flank pain. J Urol. Sep 1999;162(3 Pt 1):685-7. [Medline].
2. Borghi L, Schianchi T, Meschi T, et al. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med. Jan 10 2002;346(2):77-84. [Medline].
3. Taylor EN, Curhan GC. Fructose consumption and the risk of kidney stones. Kidney Int. Jan 2008;73(2):207-12. [Medline].
4. Avci Z, Koktener A, Uras N, et al. Nephrolithiasis associated with ceftriaxone therapy: a prospective study in 51 children. Arch Dis ChildNov. 2004;89(11):1069-72. [Medline].
5. Khositseth S, Gillingham KJ, Cook ME, Chavers BM. Urolithiasis after kidney transplantation in pediatric recipients: a single center report. Transplantation. 2004;78(9):1319-23. [Medline].
6. Barratt TM, Duffey PG. Nephrocalcinosis and Urolithiasis. 4^th ed. Philadelphia, PA: Lippincott-Raven; 1999.
7. Catalano-Pons C, Bargy S, Schlecht D, et al. Sulfadiazine-induced nephrolithiasis in children. Pediatr Nephrol. 2004;19(8):928-31. [Medline].
8. Harmon EP, Neal DE, Thomas R. Pediatric urolithiasis: review of research and current management. Pediatr Nephrol. Aug 1994;8(4):508-12. [Medline].
9. Knoll T, Zollner A, Wendt-Nordahl G, et al. Cystinuria in childhood and adolescence: recommendations for diagnosis, treatment, and follow-up. Pediatr Nephrol. 2005;20(1):19-24. [Medline].
10. Langman CB, Moore ES, Edelmann CM Jr, eds. Pediatric urolithiasis. In: Pediatric Kidney Disease. Vol 2. Philadelphia, PA: Lippincott Williams & Wilkins; 1992:2005-14.
11. Meier KH, Olson KR, Olson JL. Acute felbamate overdose with crystalluria. Clin Toxicol. 2005;43(3):189-92. [Medline].
12. Schenkman NA, Stoller ML. Urinary stone disease. In: Conn's Current Therapy. ed. Philadelphia, PA: WB Saunders Co; 1999:741.

Article Last Updated: Jul 22, 2008