What are the management options for renal stones?

Management of Renal Stones

Renal stone management requires a comprehensive approach combining initial evaluation with stone analysis and metabolic testing, followed by aggressive dietary modifications (particularly high fluid intake to achieve >2.5L urine output daily), and stone-type-specific pharmacological therapy guided by 24-hour urine metabolic profiles.

Initial Evaluation and Risk Stratification

• Obtain stone analysis at least once when available to guide specific preventive measures and determine stone composition (calcium oxalate, calcium phosphate, uric acid, cystine, or struvite) 1
• Perform metabolic testing with 24-hour urine collections in all recurrent stone formers and high-risk first-time formers, analyzing for total volume, pH, calcium, oxalate, uric acid, citrate, sodium, potassium, and creatinine 1
• Review imaging studies to quantify stone burden and identify patients at higher risk of recurrence 1
• Obtain serum intact parathyroid hormone level if primary hyperparathyroidism is suspected based on hypercalciuria and elevated serum calcium 1

Universal Dietary Management (All Stone Types)

Hydration

• Increase fluid intake to achieve at least 2.5 liters of urine output daily as the single most important intervention across all stone types 1
• For cystine stones specifically, target even higher fluid intake of at least 4 liters per day to decrease urinary cystine concentration below 250 mg/L 2
• Maintain neutral or slightly alkaline urine through adequate hydration 3

General Dietary Modifications

• Maintain normal dietary calcium intake of 1,000-1,200 mg per day for calcium stone formers—calcium restriction is contraindicated as it paradoxically increases stone risk 1
• Limit sodium intake to 2,300 mg (100 mEq) daily to reduce urinary calcium excretion and enhance efficacy of other treatments 1
• Consume ample fruits and vegetables to counterbalance dietary acid load and increase urinary citrate 1
• Limit animal protein intake to 0.8-1.0 g/kg body weight per day, as excessive protein increases calciuria, uric acid, and oxalate excretion while decreasing citrate 4

Stone-Type-Specific Pharmacological Management

Calcium Stones with Hypercalciuria

• Offer thiazide diuretics (hydrochlorothiazide or chlorthalidone) as first-line therapy, continuing dietary sodium restriction to maximize the hypocalciuric effect 1
• Monitor for hypokalemia as a common adverse effect of thiazide therapy 1
• Thiazides combined with potassium citrate may be used when other metabolic abnormalities are absent or adequately addressed but stone formation persists 5

Calcium Stones with Hypocitraturia

• Offer potassium citrate therapy to patients with low or relatively low urinary citrate (Grade B evidence from prospective RCTs) 5
• Potassium citrate is preferred over sodium citrate because sodium load increases urinary calcium excretion 5
• Increased fluid intake, sodium restriction, fruits/vegetables, and thiazides may enhance citrate therapy safety and efficacy 5
• Monitor for hyperkalemia in patients on potassium citrate, particularly those with renal impairment 1

Calcium Oxalate Stones with Hyperuricosuria

• Offer allopurinol to patients with hyperuricosuria (>800 mg/day) and normal urinary calcium (Grade B evidence from prospective RCT) 5
• Hyperuricemia is not required for allopurinol therapy—the indication is based on urinary uric acid excretion 5
• Dosing: 200-300 mg/day in divided doses or as single equivalent for recurrent calcium oxalate stones in hyperuricosuric patients 3
• Adjust dose based on subsequent 24-hour urinary urate determinations 3
• Reduce dose in renal impairment: 200 mg/day for creatinine clearance 10-20 mL/min; ≤100 mg/day for creatinine clearance <10 mL/min 3

Uric Acid Stones

• Offer potassium citrate as first-line therapy to raise urinary pH to approximately 6.0, as most patients have low urinary pH rather than hyperuricosuria 5
• Do NOT routinely offer allopurinol as first-line therapy because alkalinization addresses the primary defect (acidic urine), whereas reducing uric acid excretion alone will not prevent stones in patients with unduly acidic urine 5
• Allopurinol may be added if hyperuricosuria persists despite adequate urinary alkalinization 5

Cystine Stones

• First-line: High fluid intake (≥4 L/day), sodium restriction (≤2,300 mg/day), protein restriction, and potassium citrate to raise urinary pH to 7.0 2
• Second-line: Offer cystine-binding thiol drugs (tiopronin or D-penicillamine) to patients unresponsive to dietary modifications and urinary alkalinization, or those with large recurrent stone burdens 5
• Tiopronin is preferred over D-penicillamine due to better efficacy and fewer adverse events 2

Struvite Stones

• Struvite stones occur from urinary infection with urease-producing organisms and require complete surgical removal coupled with appropriate antibiotic therapy 6
• Consider acetohydroxamic acid (AHA) as a urease inhibitor in patients at high risk for recurrence or when surgery is not feasible, though extensive side effects may limit use 5

Calcium Phosphate Stones

• Offer potassium citrate therapy if hypocitraturia is present, as citrate is a potent inhibitor of calcium phosphate crystallization 5
• Exercise caution with excessive alkalinization, as calcium phosphate solubility decreases at higher pH 5

Follow-up and Monitoring

• Obtain 24-hour urine specimen within 6 months of initiating treatment to assess response to dietary and/or medical therapy 1
• After initial follow-up, obtain annual 24-hour urine specimens, or more frequently in active stone formers 1
• Monitor for medication-specific adverse effects: hypokalemia with thiazides, hyperkalemia with potassium citrate, and bone marrow suppression or hypersensitivity reactions with allopurinol 1, 3
• Use serum uric acid levels as an index when adjusting allopurinol dosing, though 24-hour urinary urate is more relevant for stone prevention 3

Common Pitfalls and Caveats

• Avoid calcium restriction in calcium stone formers—this paradoxically increases oxalate absorption and stone risk 1
• Do not use allopurinol as first-line for uric acid stones—urinary alkalinization with potassium citrate addresses the primary pathophysiology 5
• Reduce allopurinol dose in renal impairment to prevent drug accumulation and toxicity 3
• Continue colchicine or anti-inflammatory agents when initiating allopurinol until serum uric acid normalizes and acute attacks cease for several months 3
• Beware of excessive urinary alkalinization in calcium phosphate stone formers, as this can promote stone formation 5
• Monitor renal function closely when starting allopurinol in patients with pre-existing renal disease, as renal failure has been observed 3