Urine alkalinization is the most appropriate treatment for this patient with uric acid nephrolithiasis not adequately treated with increased urine output. Uric acid is an uncommon cause of nephrolithiasis (approximately 10% of cases). It is more common in hot arid climates where low urine output and acidic urine (low urine pH) are more likely. These two factors, particularly low urine pH, markedly increase the risk of uric acid stones by favoring the development of insoluble uric acid from the relatively soluble urate salt. Elevated serum urate levels, gout, and associated hyperuricosuria are other risk factors, although many patients with uric acid stones do not have these risk factors. Other comorbid risk factors for uric acid stones include diabetes mellitus, the metabolic syndrome, and chronic diarrhea. Oral hydration to maintain a urine output of at least 2 L/d is the mainstay of therapy. If this is inadequate, the next treatment is urine alkalinization (usually with potassium citrate or potassium bicarbonate) to increase the solubility of uric acid.

Treatment with xanthine oxidase inhibitors such as allopurinol to lower uric acid production is usually reserved for patients with refractory disease despite adequate urine output and urine alkalinization or those with very high 24-hour urine uric acid levels (>1000 mg/24 h [5.9 mmol/24 h]). Therefore, allopurinol is not the next treatment of choice in this patient with mild uricosuria who has not undergone a trial of urine alkalinization.

Cholestyramine binds bile salts and oxalate in the gut and is sometimes used as a treatment for kidney stones related to hyperoxaluria but would likely not benefit this patient with uric acid stones.

Thiazide diuretics, such as hydrochlorothiazide, decrease hypercalciuria by increasing proximal sodium reabsorption and passive calcium reabsorption in the kidney. However, this is a strategy for treating calcium-based nephrolithiasis and is not effective for uric acid stones.