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Urinary calculi are a relatively common condition with an annual incidence of 0.5% to 1.0% and prevalence in the U.S. of approximately 5%.1 The lifetime risk is approximated at 10% to 15% in the U.S. and other developed countries, with a male predominance of 2:1.2 The first episode for males occurs at an average age of 30 years, with a range from 20 to 50 years. After the sixth decade, incidence in men decreases, and the first occurrence is relatively rare after age 60. Women develop stones in a bimodal distribution at ages 35 and 55. Unfortunately, urinary calculi recur in 37% of patients in the first year, 50% of patients within 10 years, and 75% of patients in 20 years.3 Children <16 years constitute approximately 7% of all renal stone cases. Unique to children is a 1:1 sex distribution.4 The most common causes in pediatrics involve metabolic abnormalities (50%), urologic anomalies (20%), infection (15%), and immobilization syndrome (5%). The remainder are considered idiopathic. Ethnically, whites develop stones more frequently than blacks. Urologic stone disease is relatively rare in Native American and Asian populations.

Stone “belts” with higher prevalence of stone disease have been geographically described within North Carolina, South Carolina, Georgia, Tennessee, and Kentucky. However, no definitive causes for these belts have been identified, although dehydration due to hot temperatures, oxalate-rich iced tea, and protein-rich diets have been suggested as potential explanations.

Stone formation is a multistep process that includes supersaturation of the urine with urinary solutes, lack of inhibitory substances, and urinary stasis. To develop a stone, dissolved salts must supersaturate the urine and condense into a solid phase. Increasing the amount of solvent (urine) and decreasing the amount of solute (i.e., calcium, uric acid) can aid in prevention.5 Inhibitory substances, such as citrate, magnesium, and Tamm Horsfall mucoprotein (also called uromodulin, an abundant urine protein), can prevent crystal precipitation and stone formation. One small study showed lower concentration of inhibitors in stone-forming patients.6 Free flow of urine can help increase the amount of solvent and wash away crystals that have not yet formed stones. Accordingly, stasis of urine is the last element needed for the formation of a stone. Stasis can be in the form of a neurogenic bladder, due to an anatomic abnormality, the presence of foreign bodies (e.g., suture), or occur on Randall’s plaque, a collection of interstitial suburothelial calcium phosphate particles on the surface of the renal papillae.7

Approximately 75% to 80% of calculi are composed of calcium, occurring in conjunction with oxalate, phosphate, or a combination of both. These stones may develop as a result of increased urinary excretion of a given solute. Calcium excretion is elevated in conditions that include hyperparathyroidism, absorptive and renal hypercalciuria, and immobilization syndrome. Oxalate excretion is enhanced in patients with inflammatory bowel disease and as a result of small-bowel resection or jejunoileal bypass.

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