Pediatrics in Review
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(Pediatrics in Review. 1999;20:280-283. doi:10.1542/10.1542/pir.20-8-280)
© 1999 American Academy of Pediatrics

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Renal Stones

Donna Elliott, MD, MSEd*
Lawrence M. Opas, MD{dagger}

* Associate Professor of Clinical Pediatrics, University of Southern California School of Medicine; Associate Director of Pediatric Nephrology, LAC+USC Medical Center.

{dagger} Professor of Clinical Pediatrics, University of Southern California School of Medicine; Chief of Pediatric Services, Director of Pediatric Nephrology, LAC+USC Medical Center, Los Angeles, CA.


    Introduction
 
Renal stone disease is a frequent consideration in the evaluation of many kidney diseases of childhood, but the diagnosis rarely is confirmed. The true incidence is unknown; only 1 in 3,000 to 7,500 pediatric hospital admissions are attributed to renal stones. There is a bimodal peak incidence at 4 years of age and in mid-adolescence, with an equal gender prevalence. Stones are rare in African-American children. Although most renal stones in the United States have a metabolic etiology, hereditary, infectious, and dietary causes should be considered in the evaluation of affected children.


    Pathogenesis
 
Crystallization is influenced by urinary tract anatomy, flow, ion concentration, pH, and select organic and inorganic molecules. Low urinary flow rates resulting from obstruction or hypovolemia, damaged uroepithelial cells, foreign bodies, and increased ion concentration favor stone formation. Acidic urine decreases the solubility of uric acid and cystine, which promotes crystallization; an alkaline pH is conducive to the formation of struvite and calcium-containing stones. Increased urinary concentrations of citrate, pyrophosphate, glycosaminoglycans, and proteinaceous substances such as Tamm-Horsfall protein and beta2 microglobulin inhibit stone formation. Nephrocalcin, which normally is found in the urine and is known to inhibit crystal formation, frequently is absent in the urine of children who have renal stone disease.


    Infective Stones
 
Renal stones formed as a result of infection consist of an organic matrix of Tamm-Horsfall glycoprotein, struvite (Mg-NH4-PO4), and apatite (CaPO4). Urease-producing organisms such as Proteus and more rarely Pseudomonas, Klebsiella, Serratia, Staphylococcus, and Candida cause the hydrolysis of urinary urea to ammonia and carbon dioxide, creating an alkaline environment that favors crystallization.

Infective stones are more common among males and usually are detected before age 5 years; 93% of children have active infection at the time of diagnosis. Only one third of children have primary obstructive uropathy, such as posterior urethral valves, . . . [Full Text of this Article]


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