Preventative measures depend on the type of<unk> s. In those with calcium<unk> s, drinking plenty of fluids, thiazide diuretics and citrate are effective as is allopurinol in those with high uric acid levels in the blood or urine. Dietary measures Specific therapy should be tailored to the type of<unk> s involved. Diet can have an effect on the development of<unk><unk> s. Preventive strategies include some combination of dietary modifications and medications with the goal of reducing the excretory load of calculogenic compounds on the<unk> s. Dietary recommendations to minimize the formation of<unk><unk> s include * increasing total fluid intake to more than two liters per day of urine output; * limiting cola, including sugar-sweetened soft drinks; to less than one liter per week. * limiting animal protein intake to no more than two meals daily (an association between animal protein and recurrence of<unk><unk> s has been shown in men); * increasing citric acid intake, including from lemon and lime juice. Maintenance of dilute urine by means of vigorous fluid therapy is beneficial in all forms of<unk><unk> s, so increasing urine volume is a key principle for the prevention of<unk><unk> s. Fluid intake should be sufficient to maintain a urine output of at least per day. A high fluid intake may reduce the likelihood of<unk><unk>  recurrence or may increase the time between<unk>  development without unwanted effects. However, the evidence supporting these findings is uncertain. Calcium binds with available oxalate in the gastrointestinal tract, thereby preventing its absorption into the bloodstream, and reducing oxalate absorption decreases<unk><unk>  risk in susceptible people. Because of this, some doctors recommend chewing calcium tablets during meals containing oxalate foods. Calcium citrate supplements can be taken with meals if dietary calcium cannot be increased by other means. The preferred calcium supplement for people at risk of<unk>  formation is calcium citrate because it helps to increase urinary citrate excretion. Aside from vigorous oral hydration and eating more dietary calcium, other prevention strategies include avoidance of large doses of supplemental and restriction of oxalate-rich foods such as leaf vegetables, rhubarb, soy products and chocolate. However, no randomized, controlled trial of oxalate restriction has been performed to test the hypothesis that oxalate restriction reduces<unk>  formation. Some evidence indicates magnesium intake decreases the risk of symptomatic<unk><unk> s. Urine alkalinization The mainstay for medical management of uric acid<unk> s is alkalinization (increasing the pH) of the urine. Uric acid<unk> s are among the few types amenable to dissolution therapy, referred to as chemolysis. Chemolysis is usually achieved through the use of oral medications, although in some cases, intravenous agents or even instillation of certain irrigating agents directly onto the<unk>  can be performed, using antegrade nephrostomy or retrograde ureteral catheters. Acetazolamide is a medication that alkalinizes the urine. In addition to acetazolamide or as an alternative, certain dietary supplements are available that produce a similar alkalinization of the urine. These include sodium bicarbonate, potassium citrate, magnesium citrate, and Bicitra (a combination of citric acid monohydrate and sodium citrate dihydrate). Aside from alkalinization of the urine, these supplements have the added advantage of increasing the urinary citrate level, which helps to reduce the aggregation of calcium oxalate<unk> s. Increasing the urine pH to around 6.5 provides optimal conditions for dissolution of uric acid<unk> s. Increasing the urine pH to a value higher than 7.0 increases the risk of calcium phosphate<unk>  formation. Testing the urine periodically with nitrazine paper can help to ensure the urine pH remains in this optimal range. Using this approach,<unk>  dissolution rate can be expected to be around of<unk>  radius per month. Slaked lime It decreases urinary calcium when combined with food rich in oxalic acid such as green leafy vegetables. Diuretics One of the recognized medical therapies for prevention of<unk> s is the thiazide and thiazide-like diuretics, such as chlorthalidone or indapamide. These drugs inhibit the formation of calcium-containing<unk> s by reducing urinary calcium excretion. Sodium restriction is necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Thiazides work best for renal leak hypercalciuria (high urine calcium levels), a condition in which high urinary calcium levels are caused by a primary<unk>  defect. Thiazides are useful for treating absorptive hypercalciuria, a condition in which high urinary calcium is a result of excess absorption from the gastrointestinal tract. Allopurinol For people with hyperuricosuria and calcium<unk> s, allopurinol is one of the few treatments that have been shown to reduce<unk><unk>  recurrences. Allopurinol interferes with the production of uric acid in the liver. The drug is also used in people with gout or hyperuricemia (high serum uric acid levels). Dosage is adjusted to maintain a reduced urinary excretion of uric acid. Serum uric acid level at or below 6 mg/100 ml) is often a therapeutic goal. Hyperuricemia is not necessary for the formation of uric acid<unk> s; hyperuricosuria can occur in the presence of normal or even low serum uric acid. Some practitioners advocate adding allopurinol only in people in whom hyperuricosuria and hyperuricemia persist, despite the use of a urine-alkalinizing agent such as sodium bicarbonate or potassium citrate.
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