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INTRODUCTION AND EPIDEMIOLOGY

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.” Renal stones in children are discussed in Chapter 133, “Acute Abdominal Pain in Infants and Children.”

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 also documented in Europe and Southeast Asia.3 Obesity and diabetes are strongly associated with kidney stones.2 For first-time stone formers, recurrence rates at 2, 5, 10, and 15 years are 11%, 20%, 31%, and 39%, respectively.4

PATHOPHYSIOLOGY

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. 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), which are found most commonly in women with recurrent urinary tract infections. 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, occurs more commonly in men, and is associated with gout or chemotherapy. Urate stones are radiolucent, and the urine is typically acidic. Cystine stones account for approximately 1% of all stones and occur in patients with cystinuria, an autosomal recessive genetic disorder affecting amino acid transport (COLA: cysteine, ornithine, lysine, arginine).

Some medications predispose to stone disease. The protease inhibitor indinavir sulfate, used to treat the human immunodeficiency virus, is associated with a 4% to 10% incidence of symptomatic urolithiasis. Pure indinavir stones are radiolucent on plain abdominal radiograph and CT scan. Carbonic anhydrase inhibitors, triamterene, and laxative abuse also increase the prevalence of ...

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