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Emergency medicine management is directed at relieving pain, assessing kidney function, and determining the likelihood of spontaneous stone passage. This chapter discusses renal and ureteral stones. Bladder stones are discussed in chapter 92, "Acute Urinary Retention."

The prevalence of kidney stones in the United States has risen from 5.2% in 19941 to 8.8% in 2010.2 The prevalence is 10.6% in men and 7.1% in women.2 Increasing prevalence is documented in Europe and Southeast Asia.3 Obesity and diabetes are strongly associated with kidney stones.2 The lifetime risk is approximated at 10% to 15% in the United States and other developed countries. Urinary calculi recur in 37% of patients in the first year, 50% of patients within 10 years, and 75% of patients in 20 years.4 Children <16 years old constitute about 7% of all renal stone cases.5 Unique to children is a 1:1 sex distribution.4 The most common causes in children involve metabolic abnormalities (50%), urologic anomalies (20%), infection (15%), immobilization syndrome (5%), and idiopathic causes (10%).5 Ethnically, whites develop stones more frequently than blacks.2


Stone formation requires supersaturation of dissolved salts in the urine, which condense into a solid phase. Increasing the amount of solvent (urine) and decreasing the amount of solute presented to the kidney (i.e., calcium, oxalate, uric acid) can aid in prevention. Inhibitory substances, such as citrate, and magnesium can prevent crystal precipitation and stone formation.

About 80% of calculi are composed of calcium oxalate, calcium phosphate, or a combination of both. Calcium excretion is elevated in conditions that include hyperparathyroidism, absorptive and renal hypercalciuria, and immobilization syndrome. Randall's plaque, a collection of interstitial suburothelial calcium phosphate particles on the surface of the renal papillae, serves as a nucleation surface for calcium oxalate stones.6,7 Complex interactions between the gut, kidney, and bones contribute to calcium oxalate stone formation. A diet restricting calcium paradoxically increases calcium stone formation because there is less calcium to bind oxalate in the intestinal lumen, leading to increased absorption of oxalate from the gut, recruitment of calcium from bones, osteoporosis, and symptomatic stone disease in predisposed patients.

About 10% of stones are struvite (magnesium-ammonium-phosphate). These stones are associated with infection by urea-splitting bacteria (Proteus, Klebsiella, Staphylococcus species, Providencia, and Corynebacterium) and are the most common cause of staghorn calculi, which are large stones that form a cast of the renal pelvis. Antibiotic penetration into staghorn calculi is poor, and the potential for urosepsis exists as long as the stones remain.

Uric acid causes about 10% of urolithiasis. Twenty-five percent of patients with gout will develop kidney stones, and they occur at a rate of approximately 1% per year after the first gout attack. Urate stones are radiolucent, and the urine is typically ...

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