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Urolithiasis is the term used to describe the presence of a stone or a calculus anywhere in the urinary tract. Nephrolithiasis is the term generally used when calculi are found in the kidneys; it should not be confused with nephrocalcinosis, which is the deposition of calcium in the tubulointerstitial regions of the kidneys. The prevalence of urolithiasis varies widely with geography. Although uncommon in some countries, it remains an important childhood condition as it is often associated with morbidity and high rates of recurrence, especially in children in whom there is an identified metabolic or genetic disorder or an underlying abnormality of the urinary tract. A thorough evaluation should be done to identify specific metabolic defects or predisposing factors to stone formation.


Although the true incidence of stones in children is unknown, it is becoming clear that the incidence is increasing. Current estimates suggest that nephrolithiasis is responsible for 1 in 685 pediatric hospital admissions in the United States. The incidence of urolithiasis has increased in all pediatric and adolescent groups over the past 10 years, especially in adolescent girls where the incidence effectively doubled from 1997 to 2012. The reasons for this dramatic increase in the incidence of stones are likely multiple and may be related to dietary factors, obesity, decreased water intake, and better detection by imaging modalities. Urolithiasis in many children probably remains undiagnosed, especially if it is asymptomatic. Stones were generally more common in white than African American or Asian children and in males; however, this race divide is narrowing, especially in North America, and girls are now more commonly affected than boys. In North America, most stones are found in the kidney. Bladder stones occur in less than 10% of affected children and are usually related to underlying urologic abnormalities.


The process of stone formation begins with the crystallization of solutes. Aggregation with other crystals and adherence to renal tubular cells are important next steps. The crystallization and aggregation of solutes depend on urinary solute concentration, urinary pH, and the presence of inhibitors of stone formation in the urine. Increased solute concentration (resulting from increased urinary excretion or low urinary volume) combined with low levels of natural inhibitors of stone formation, including citrate, magnesium, and pyrophosphate, will predispose to stone formation. A decrease in water intake will increase the urinary saturation of the stone-forming products calcium, phosphate, and oxalate. A diet rich in salt will promote hypercalciuria, and a diet low in calcium favors absorption of oxalate from the gastrointestinal tract, thereby increasing urinary oxalate excretion.


Metabolic risk factors include hypercalciuria, hypocitraturia, hyperoxaluria, hypomagnesuria, and hyperuricosuria. Structural abnormalities of the urinary tract and urinary tract infections also predispose to renal stone formation. There are also an increasing number of inherited monogenic diseases associated with recurrent renal stone formation.

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