Approach to Metabolic Stone Disease
All stone formers require a systematic evaluation beginning with screening tests, followed by metabolic testing in high-risk patients, and targeted dietary plus pharmacologic therapy based on stone composition and 24-hour urine abnormalities. 1
Initial Screening Evaluation (All Stone Formers)
Perform these baseline assessments in every patient with kidney stones: 1
Detailed medical and dietary history focusing on stone-provoking medications, supplements, fluid intake (amount and specific beverages), protein types and amounts, calcium, sodium, high-oxalate foods, fruits, vegetables, and over-the-counter supplements 1
Serum chemistries including electrolytes, calcium, creatinine, and uric acid to identify underlying metabolic conditions 1
Serum intact parathyroid hormone if calcium is high or high-normal to rule out primary hyperparathyroidism 1
Urinalysis with both dipstick and microscopic examination to assess urine pH, detect infection, and identify pathognomonic crystals 1
Urine culture if urinalysis suggests infection or patient has recurrent UTIs 1
Stone analysis at least once when stone is available, as composition (uric acid, cystine, struvite) directly guides preventive therapy 1, 2
Review imaging studies to quantify total stone burden; multiple/bilateral stones or nephrocalcinosis indicate higher recurrence risk and underlying metabolic disorders 1, 2
Risk Stratification
Identify high-risk stone formers who require metabolic testing: 1, 3
- Recurrent stone formers (≥2 stones)
- Multiple or bilateral stones at presentation
- Nephrocalcinosis on imaging
- Stone composition of uric acid, cystine, or struvite
- First-time formers who are interested in prevention
- Associated systemic conditions (obesity, hypertension, diabetes)
Metabolic Testing (High-Risk Patients)
Obtain one or two 24-hour urine collections on a random diet analyzing for: 1, 2
- Total volume
- pH
- Calcium
- Oxalate
- Uric acid
- Citrate
- Sodium
- Potassium
- Creatinine
Additional testing considerations: 1, 2
- Measure urinary cystine if cystine stones are known, family history of cystinuria exists, or cystinuria is suspected 1
- Suspect primary hyperoxaluria when urinary oxalate exceeds 75 mg/day without bowel dysfunction 1
Universal Dietary Interventions (All Stone Formers)
These dietary modifications apply regardless of stone type: 1, 2, 4
- Increase fluid intake to achieve urine output of at least 2.5 liters daily—this is the single most critical intervention across all stone types 2, 4
- Maintain normal dietary calcium intake of 1,000-1,200 mg/day; do not restrict calcium as this paradoxically increases stone risk by enhancing intestinal oxalate absorption 2, 5
- Limit sodium intake to 2,300 mg (100 mEq) daily to reduce urinary calcium excretion 2, 5
- Reduce animal protein intake, as high consumption increases stone risk 1, 6
- Increase fruits and vegetables intake 1, 6
- Avoid supplemental calcium; use dietary sources only 5
Stone Type-Specific Pharmacologic Therapy
Calcium Oxalate/Calcium Phosphate Stones
For hypercalciuria (high or relatively high urine calcium): 1, 2, 5
- Offer thiazide diuretics (hydrochlorothiazide 25 mg twice daily or 50 mg once daily) combined with continued sodium restriction 2, 5
For hypocitraturia (low or relatively low urinary citrate): 1, 2, 5
- Offer potassium citrate therapy at 30-80 mEq/day in 3-4 divided doses to increase urinary citrate 2, 5
For hyperoxaluria: 1
- Restrict dietary oxalate intake (chocolate, nuts, spinach, rhubarb) 1
- Ensure adequate dietary calcium to bind intestinal oxalate 2
Uric Acid Stones
First-line therapy is urinary alkalinization, not allopurinol: 2, 5, 4
- Potassium citrate to raise urinary pH to approximately 6.0-6.5, enhancing uric acid solubility 2, 5, 4
- Allopurinol 200-300 mg/day is reserved for hyperuricosuric calcium oxalate stone formers, not primary uric acid stones 5, 7
Cystine Stones
Aggressive multimodal approach required: 2, 5
- Increase fluid intake to at least 4 liters/day to decrease urinary cystine concentration below 250 mg/L 2
- Urinary alkalinization with potassium citrate to target pH >7.0 5
- Restrict sodium and protein intake 5
- Penicillamine or tiopronin if conservative measures fail 8
Struvite (Infection) Stones
Stone removal is essential: 2
- Surgical removal to limit recurrent UTI and prevent renal damage 2
- Antimicrobial therapy based on culture results 2
Brushite (Calcium Phosphate) Stones
For hypocitraturia or elevated urine pH: 5
- Potassium citrate as first-line therapy 5
- Thiazide diuretics if hypercalciuria is present 5
- Combination therapy for persistent stone formation 5
Follow-Up and Monitoring
Structured follow-up is essential to assess treatment response: 1, 2, 5
- Obtain 24-hour urine specimen within 6 months of initiating dietary and/or medical therapy to assess response 2, 5
- Annual 24-hour urine collections after initial follow-up, or more frequently if stone activity persists 2, 5
- Periodic blood testing to monitor for adverse effects of pharmacologic therapy (electrolytes, glucose, renal function) 2, 5
- Repeat stone analysis when available, especially if not responding to treatment 2, 5
- Serial imaging to assess for new stone formation or growth of existing stones 2
- Adjust therapy based on urinary parameters and patient adherence 2
Critical Pitfalls to Avoid
- Never restrict dietary calcium—this increases intestinal oxalate absorption and stone risk 2, 5, 4
- Never use allopurinol as first-line therapy for uric acid stones—urinary alkalinization with potassium citrate is superior 5, 4
- Never use supplemental calcium instead of dietary calcium—supplements may increase stone formation risk 5
- Never neglect stone analysis—composition directly determines appropriate therapy 1, 2
- Never skip metabolic testing in high-risk patients—specific therapy based on 24-hour urine abnormalities is more effective than general measures 1, 3
- Never forget that fluid intake is the single most important intervention—target at least 2.5 liters of urine output daily across all stone types 2, 4