Pediatric Urolithiasis Medication

  • Author: Sahar Fathallah-Shaykh, MD; Chief Editor: Craig B Langman, MD   more...
 
Updated: May 4, 2012
 

Medication Summary

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.

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Alkalinizing Agents

Class Summary

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.

Sodium citrate/citric acid (Cytra-2, Liqui-DualCitra)

 

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)

 

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).

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Diuretics

Class Summary

These agents are used to decrease urinary calcium excretion.

Hydrochlorothiazide (Microzide, Oretic)

 

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.

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Xanthine oxidase inhibitors

Class Summary

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.

Allopurinol (Zyloprim, Aloprim)

 

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.

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Contributor Information and Disclosures
Author

Sahar Fathallah-Shaykh, MD  Assistant Professor in 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 and American Society of Pediatric Nephrology

Disclosure: emedecine Honoraria Other

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 & Dental Society, 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, and Southwest Pediatric Nephrology Study Group

Disclosure: The Osler Institute Honoraria Speaking and teaching

Specialty Editor Board

Deogracias Pena, MD  Medical Director of Dialysis, Department of Pediatrics, Cook Children's Medical Center; Clinical Associate Professor, Texas Tech University School of Medicine

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

Disclosure: Nothing to disclose.

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, and 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, Children's Memorial Hospital

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

Disclosure: NIH Grant/research funds None; Raptor Pharmaceuticals, Inc Grant/research funds None; Alexion Pharmaceuticals, Inc. Grant/research funds None

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. Jan 10 2002;346(2):77-84. [Medline].

  2. Taylor EN, Curhan GC. Fructose consumption and the risk of kidney stones. Kidney Int. Jan 2008;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. 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. Feb 22 2012;[Medline].

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

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

  8. 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].

  9. Schwaderer AL, Cronin R, Mahan JD, Bates CM. Low bone density in children with hypercalciuria and/or nephrolithiasis. Pediatr Nephrol. Dec 2008;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/ephedrineDrug 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, acetazolamideCalcium phosphate
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