Management of Uric Acid and Calcium Oxalate Stones
Uric Acid Stones
Potassium citrate is the first-line therapy for uric acid stones, targeting a urinary pH of 6.0-6.5 to dissolve existing stones and prevent recurrence. 1, 2
Primary Treatment Strategy
Urinary alkalinization with potassium citrate is the cornerstone of management because most uric acid stone formers have unduly acidic urine (pH <5.5) rather than hyperuricosuria as the primary problem. 1, 2, 3
The target urinary pH should be 6.0-6.5; this significantly increases uric acid solubility and can dissolve existing stones. 2, 3
Allopurinol should NOT be used as first-line therapy for uric acid stones unless hyperuricosuria is documented, as reducing uric acid excretion will not prevent stones in patients with acidic urine. 1, 2
Potassium citrate is preferred over sodium citrate because sodium loading may increase urinary calcium excretion and promote mixed stone formation. 1, 2
Dosing and Monitoring
For uric acid stones, potassium citrate should be initiated at 30-60 mEq/day divided with meals, with the goal of raising urinary pH to 6.0-7.0. 4
Critical pitfall: Avoid raising urinary pH above 7.0, as this increases the risk of calcium phosphate stone formation. 2
Obtain 24-hour urine testing within 6 months of initiating treatment to assess metabolic response, then annually. 1
Adjunctive Measures
Fluid intake should be sufficient to produce at least 2 liters of urine output daily. 2, 4, 3
Sodium restriction (target ≤2,300 mg/day) helps prevent mixed stones by reducing urinary calcium excretion. 2
Maintain normal dietary calcium intake (1,000-1,200 mg/day) to bind oxalate in the gut and prevent calcium oxalate component formation. 2
Calcium Oxalate Stones
For calcium oxalate stones, management focuses on increasing fluid intake, normalizing dietary calcium (1,000-1,200 mg/day), restricting sodium, and using potassium citrate for hypocitraturia. 5, 1
Dietary Management
Counsel patients to consume 1,000-1,200 mg/day of dietary calcium from food sources, as higher dietary calcium intake independently reduces stone risk by binding intestinal oxalate. 5, 6
Limit sodium intake to ≤2,300 mg/day (100 mEq), as dietary sodium increases urinary calcium excretion. 5
Important caveat: Calcium supplements may increase stone risk (20% higher in one observational study), unlike dietary calcium; supplements should only be used if dietary sources are inadequate. 5
For patients with high urinary oxalate, limit oxalate-rich foods while maintaining normal calcium consumption; calcium should be consumed primarily at meals to enhance gastrointestinal oxalate binding. 5
Patients with enteric hyperoxaluria (inflammatory bowel disease, gastric bypass) may require more restrictive oxalate diets and higher calcium intakes, including supplements timed with meals. 5
Pharmacologic Management
Offer potassium citrate to patients with hypocitraturia (urinary citrate <320 mg/day), as prospective RCTs demonstrate reduced stone recurrence. 1
Potassium citrate should also be offered to patients with normal citrate but low urinary pH, as it inhibits calcium oxalate and calcium phosphate crystallization. 1
Thiazide diuretics should be offered to patients with high or relatively high urinary calcium and recurrent stones; hydrochlorothiazide 25 mg orally is associated with hypocalciuric effect. 5
Fluid and Monitoring
Increase fluid intake to achieve at least 2 liters of urine output daily; this is the single most important intervention across all stone types. 5, 6
Obtain 24-hour urine collection to measure volume, pH, calcium, oxalate, citrate, uric acid, and sodium to guide targeted therapy. 5, 1
Follow-up metabolic testing should occur within 6 months of treatment initiation, then annually or more frequently based on stone activity. 1
Special Considerations for Mixed Stones
When hyperuricosuria is present with calcium oxalate stones, allopurinol 200-300 mg/day may be beneficial, as uric acid can promote calcium oxalate crystallization. 7, 8
For mixed uric acid and calcium oxalate stones, potassium citrate addresses both components by raising pH and increasing citrate. 2