eMedicine Specialties > Urology > Stones

Hyperuricosuria and Gouty Diathesis: Treatment & Medication

Author: Bijan Shekarriz, MD, Director, Laparoscopy and Minimally Invasive Surgery, Associate Professor of Urology, Department of Urology, State University of New York Upstate Medical University
Coauthor(s): Marshall L Stoller, MD, Medical Director of Urinary Stone Center, Professor, Department of Urology, University of California at San Francisco; Brian H Eisner, MD, Instructor in Surgery, Department of Urology, Massachusetts General Hospital-Harvard Medical School; Fellow in Endourology, Department of Urology, University of California
Contributor Information and Disclosures

Updated: Jul 28, 2008

Treatment

Medical Care

In the acute phase, the primary goals are symptomatic relief with hydration for the euvolemic state and adequate pain management. When the acute stone episode has resolved, the cornerstones of medical treatment are urinary alkalinization (ie, pH 6.5-7.0), hydration (ie, urinary output 1500-2000 mL/d), and allopurinol (ie, patients with hyperuricosuric calcium nephrolithiasis) to decrease serum and urinary uric acid levels. The authors have observed impressive dissolution of large uric acid stones (staghorn) with oral alkalinization (see Images 1-2). These measures are effective for dissolving existing uric acid stones and for stone prophylaxis.

Surgical Care

In the acute phase, surgical intervention may be indicated to relieve urinary obstruction associated with infection or to relieve pain in patients who are not responding to medical treatment. Furthermore, a complete or high-grade ureteral obstruction may require intervention irrespective of the clinical symptoms. In all these circumstances, the urinary obstruction should be relieved. This may be achieved by retrograde insertion of a ureteral stent or a percutaneous nephrostomy tube.

• Once the acute stone event has subsided, urinary alkalinization is the treatment of choice for dissolution of uric acid stones. Percutaneous or retrograde irrigation with alkalinizing agents was a common practice in the past. It was mainly used for dissolution of residual stone fragments after percutaneous or retrograde manipulations or in patients who did not tolerate systemic alkalinization. The most commonly used solutions are sodium bicarbonate (pH 7.0-8.0), tromethamine (THAM, pH 8.6), and 0.3 M tromethamine E (THAM-E, pH 10.5). These procedures require prolonged hospitalization and are currently not cost-effective compared with modern endourological modalities.
• Surgical intervention (eg, percutaneous nephrolithotomy) may be necessary for treating large uric acid stones that do not dissolve with medical management.
• Hyperuricosuric calcium stones are not amenable to chemolysis; surgical intervention may be indicated based on stone size.
• Extracorporeal shockwave lithotripsy (ESWL) is the primary mode of treatment for renal and proximal ureteral stones up to 2.5 cm in maximal diameter. Uric acid stones fragment easily with ESWL, and this modality may improve oral chemolysis by increasing the stone surface. Larger stones may require percutaneous nephrolithotripsy. Intravenous or retrograde contrast via ureteral catheters or double-J stents may be necessary for visualization of the uric acid calculi during ESWL.
• Ureteroscopy and intracorporeal lithotripsy are the treatments of choice for most large or impacted distal ureteral stones. All intracorporeal lithotripsy modalities, such as electrohydraulic, ultrasonic, or laser, are effective for uric acid stone fragmentation.

Consultations

• Internal medicine specialist for gout
• Oncologist for management of myeloproliferative disease

Diet

A diet with high fluid intake, low sodium intake, and moderate protein intake is recommended. Low sodium intake reduces sodium urinary excretion, which reduces monosodium urates that are catalysts for hyperuricosuric calcium nephrolithiasis. Additionally, decreased sodium intake reduces sodium urinary excretion, which reduces urinary calcium excretion.

Activity

Individuals with sedentary and white-collar occupations are at an increased risk for urinary stones; therefore, regular physical exercise may be beneficial in all persons who form stones. Physical activity may facilitate stone passage during acute renal colic.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Urinary alkalinizing agents

The most important medications used for the dissolution or prevention of uric acid urinary stones are alkalinizing agents (eg, potassium citrate) to increase the urinary pH to 6.5-7.0. Balanced citrate alkali (eg, potassium citrate; Urocit-K, Polycitra-K) are the most commonly used medications. Sodium and potassium bicarbonate are also used frequently. One disadvantage of sodium alkali is that the increased sodium and fluid load may be detrimental to patients with renal failure, liver failure, or congestive heart failure.

Alternatively, citrate supplementation may be given. Citrate inhibits calcium oxalate crystallization directly and by complexing with calcium in solution to reduce its concentration and availability. Potassium citrate is preferred over sodium citrate because it is not associated with a sodium load. Potassium citrate comes in a slow-release wax-based tablet, which may be seen as an intact tablet in the stool; however, the citrate has been absorbed. Patients should be warned that this may occur.

For patients who are not tolerant of or compliant with a frequent dosing schedule, a single evening dose may be quite beneficial to increase the urinary pH (alkaline tide) overnight.

Potassium citrate can also be given as a crystal preparation. The advantage of this preparation is that it forces patients to increase their fluid intake. Potassium citrate may be given in liquid preparations, with and without glucose additives. Finally, lemonade has been shown to increase urinary citrate levels and is an alternative or supplement to pharmacologic formulations.

The primary treatment for uric acid stones is urinary alkalinization. Surprisingly, it is not associated with hypocitraturia. Allopurinol should be added to the therapeutic regimen in the presence of associated hyperuricemia, hyperuricosuric calcium stone disease, intolerance of alkali, or continuing uric acid stone production despite alkalinization therapy. Initial dosing should be 300 mg/d.

Potassium citrate (Urocit-K, Polycitra-K)

Available as tab, syr, and crystals. All forms should be taken with water or juice according to directions.

Potassium bicarbonate and potassium citrate (Effer-K, K-Ide, Klor-Con/EF, K-Lyte

Needed for conduction of nerve impulses in heart, brain, and skeletal muscle. Helps maintain normal renal function. Plays role in contraction of cardiac, skeletal, and smooth muscles. All PO forms of potassium bicarbonate should be taken with adequate fluids according to directions.

Sodium bicarbonate (Neut)

Excellent urinary alkalinization agent. Dissociates to provide bicarbonate ion, which neutralizes hydrogen ion concentration and raises blood and urinary pH.

Antihyperuricemic agents

In cases of hyperuricemia or significant hyperuricosuria, allopurinol is effective. This drug inhibits the conversion of hypoxanthine and xanthine to uric acid. In patients with hyperuricosuric calcium stones, treatment involves reducing the monosodium urate–induced calcium oxalate crystallization. This is accomplished by decreasing urinary uric acid excretion and limiting dietary sodium intake (<150 mEq/d). Patients should initially be treated with dietary purine and sodium restriction. In approximately 30% of patients, hyperuricosuria is due to uric acid overproduction and does not improve with dietary restriction. In this situation and in patients intolerant of diet restriction, allopurinol is the medication of choice.

Allopurinol (Zyloprim)

Inhibits xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine. Reduces the synthesis of uric acid without disrupting the biosynthesis of vital purines.

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