Review articleMedical management of pediatric stone disease
Section snippets
Manifestations
Clinical manifestations of stone disease are often more subtle in children, particularly younger children, when compared with the dramatic adult presentation with incapacitating pain. Abdominal, flank, or pelvic pain occurs as the initial clinical feature in approximately 50% of children with urolithiasis [3], [9], whereas gross or microscopic hematuria leads to the diagnosis in 33%, incidental radiographic findings in 15%, and infection in 11% [3]. In infancy, pain from stones may mimic colic.
Etiology
As is true in adults, greater than 75% of all urinary tract calculi reported in North American children are composed of calcium oxalate or calcium phosphate [3], [12]. Infection stones, which represent 15% to 25% of the total, are the second most common form of calculosis [3], [5], [6], [7]. The published etiology of renal stones in childhood varies depending on the source of the review, namely, a surgical or medical population, but in two large pediatric series that included both patient
Pathophysiology
Urine is a complex solution containing ions that interact with other constituents. The generation of crystals is a process that is variably promoted or inhibited by several physicochemical or anatomic factors. These factors include the solute excretion rate, urinary supersaturation, urinary ionic strength, urinary flow rate, urine pH, and urinary tract developmental anomalies. In normal urine, the concentration of a component necessary to reach supersaturation is several times higher than would
Evaluation
The evaluation of a child who presents with urolithiasis is not unlike that performed in an adult and should be directed toward identifying any physicochemical, anatomic, and genetic factors predisposing to urolithiasis. Because 78% of all stones analyzed in children are composed of calcium oxalate or calcium phosphate [3], this finding is of limited assistance in the evaluation. Short of finding a uric acid, cystine, or struvite stone, the search for an etiology consists of blood and urine
Radiographic evaluation
Similar to the experience in adults, the search for urolithiasis in children with hypercalciuria is best accomplished by performing a nonenhanced helical CT scan, as demonstrated by Nimkin et al [16] in a study of 25 children with documented urolithiasis. CT had by far the highest sensitivity for detecting calculi when compared with renal ultrasound, IVP, or abdominal flat plate imaging. Advantages of noncontrast, thin-section, helical CT over excretory urography include shorter examination
Hypercalciuria
Hypercalciuria is the most common cause of urolithiasis in children, accounting for up to 34% of all pediatric stones [3]. Normal calcium excretion during childhood has been defined as less than 4 mg/kg per day measured in a 24-hour urine collection with the patient consuming a routine diet [20], [21], [22], preferably confirmed with a second sample. In children with documented idiopathic hypercalciuria, it is reasonable to institute a sodium-restricted diet (2–3 g/day) for 2 to 4 weeks and
Uric acid urolithiasis
Uric acid is the end product of purine metabolism. As many as 8% of children with metabolic stones have hyperuricosuria [3]. Hyperuricosuria predisposes not only to uric acid precipitation but also to calcium oxalate lithiasis, the latter by epistaxis. Two major factors promote uric acid precipitation: a high urinary concentration of uric acid and a urinary pH of less than 5.8.
Hyperuricosuria may result from uric acid overproduction, or may occur in the presence of normal serum uric acid
Struvite stones
Infection-related stones account for 2% to 24% of children with nephrolithiasis [3], [5], [6], [7], [12] and as many as 75% of stones in European children. Infection stones are more common in males and are usually detected before the age of 6 years. More than half of all children with infection-related stones have genitourinary anomalies [3]. Affected children have persistent pyuria, bacteriuria, and struvite crystalluria.
Infection stones consist of an organic matrix of Tamm-Horsfall
Cystinuria
Cystinuria accounts for 2% to 7% of children with metabolic urolithiasis in industrialized countries [3], [5]. Cystinuria is an incompletely recessive autosomal disorder characterized by failure of tubular reabsorption of four basic amino acids: cystine, ornithine, lysine, and arginine. It occurs with a frequency of approximately 1 case per 15,000 population in the United States. Only cystine has poor solubility in the normal urinary pH range. The solubility of cystine in urine is about 250
Hyperoxaluria
Oxalate is a product of human metabolism produced in the liver and excreted primarily by the kidney. Oxalate is also absorbed from the diet, and renal excretion reflects the combined endogenous and exogenous oxalate loads. Hyperoxaluria accounts for a small but significant portion of pediatric stone disease.
Primary hyperoxaluria usually presents as calcium oxalate stone formation or nephrocalcinosis during childhood. Some patients never have clinical stone disease; rather, they experience
Hypocitraturia
A decrease in the excretion of urinary inhibitors of crystal formation can promote the development of stones. A principal inhibitor of stone formation is citrate. Hypocitraturia can occur in isolation or in association with hypercalciuria, hyperuricosuria, or hyperoxaluria. Citrate excretion can be limited by chronic metabolic acidosis, induced by chronic diarrhea, RTA, or a high-protein diet, as well as hypokalemia.
Clinical disorders associated with urolithiasis in children are listed in Box 3
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