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Pediatric Urolithiasis Treatment & Management

  • Author: Sahar Fathallah-Shaykh, MD; Chief Editor: Craig B Langman, MD  more...
 
Updated: Feb 15, 2016
 

Approach Considerations

The overall goals of care are as follows:

  • To prevent additional renal damage, which may lead to loss of renal parenchyma
  • To manage pain associated current stone(s)
  • To expedite passage or removal of any stones present
  • To prevent new stones from forming.

Management may include medical approaches, surgical interventions, and dietary modification.

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Conservative Treatment

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.

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Stone Removal

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,[12] 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.[13, 14]

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Dietary Measures

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.

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Consultations

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.

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Long-Term Monitoring

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.[15]

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.

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Contributor Information and Disclosures
Author

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

Sahar Fathallah-Shaykh, MD is a member of the following medical societies: American Society of Nephrology, American Society of Pediatric Nephrology

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

Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical and Dental Associations, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, Southwest Pediatric Nephrology Study Group

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Luther Travis, MD is a member of the following medical societies: Alpha Omega Alpha, American Federation for Medical Research, International Society of Nephrology, Texas Pediatric Society

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

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Raptor Pharmaceuticals; Eli Lilly and Company; Dicerna<br/>Received grant/research funds from NIH for none; Received grant/research funds from Raptor Pharmaceuticals, Inc for none; Received grant/research funds from Alexion Pharmaceuticals, Inc. for none; Received consulting fee from DiCerna Pharmaceutical Inc. for none.

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

Deogracias Pena, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

References
  1. Borghi L, Schianchi T, Meschi T, et al. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med. 2002 Jan 10. 346(2):77-84. [Medline].

  2. Taylor EN, Curhan GC. Fructose consumption and the risk of kidney stones. Kidney Int. 2008 Jan. 73(2):207-12. [Medline].

  3. 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].

  4. 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].

  5. Johnson EK, Lightdale JR, Nelson CP. Risk factors for urolithiasis in gastrostomy tube fed children: a case-control study. Pediatrics. 2013 Jul. 132(1):e167-74. [Medline]. [Full Text].

  6. Bergsland KJ, Coe FL, White MD, Erhard MJ, Defoor WR, Mahan JD, et al. Urine risk factors in children with calcium kidney stones and their siblings. Kidney Int. 2012 Feb 22. [Medline].

  7. Routh JC, Graham DA, Nelson CP. Epidemiological trends in pediatric urolithiasis at United States freestanding pediatric hospitals. J Urol. 2010 Sep. 184(3):1100-4. [Medline].

  8. Bush NC, Xu L, Brown BJ, Holzer MS, et al. Hospitalizations for pediatric stone disease in United States, 2002-2007. J Urol. 2010 Mar. 183(3):1151-6. [Medline].

  9. Tasian GE, Ross ME, Song L, Sas DJ, Keren R, Denburg MR, et al. Annual Incidence of Nephrolithiasis among Children and Adults in South Carolina from 1997 to 2012. Clin J Am Soc Nephrol. 2016 Jan 14. [Medline].

  10. Pong YH, Huang WY, Lu YC, Tsai VF, Chen YF, Chang HC, et al. Temporal trend of newly diagnosed incidence, medical utilization, and costs for pediatric urolithiasis, 1998-2007: a nationwide population-based study in Taiwan. Urology. 2015 Jan. 85 (1):216-20. [Medline].

  11. Bove P, Kaplan D, Dalrymple N, et al. Reexamining the value of hematuria testing in patients with acute flank pain. J Urol. 1999 Sep. 162(3 Pt 1):685-7. [Medline].

  12. Dangle PP, Bandari J, Lyon TD, Lee A, Ayyash O, Cannon GM Jr, et al. Outcomes of Ureteroscopic Management of Pediatric Urolithiasis: A Comparative Analysis of Prepubertal and Adolescent Patients. Urology. 2015 Dec 30. [Medline].

  13. Erturhan S, Bayrak O, Sarica K, Seckiner I, Baturu M, Sen H. Efficacy of medical expulsive treatment with doxazosin in pediatric patients. Urology. 2013 Mar. 81(3):640-3. [Medline].

  14. Velázquez N, Zapata D, Wang HH, Wiener JS, Lipkin ME, Routh JC. Medical expulsive therapy for pediatric urolithiasis: Systematic review and meta-analysis. J Pediatr Urol. 2015 Dec. 11 (6):321-7. [Medline].

  15. Schwaderer AL, Cronin R, Mahan JD, Bates CM. Low bone density in children with hypercalciuria and/or nephrolithiasis. Pediatr Nephrol. 2008 Dec. 23(12):2209-14. [Medline].

 
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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 stones on the right is composed of cysteine.
Table 1. 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
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