Pediatric Urolithiasis Clinical Presentation

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

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 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.[8] 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).

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Physical Examination

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.

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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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