## Most Common Cause of Nephrolithiasis **Key Point:** Hypercalciuria accounts for approximately 40–50% of all idiopathic calcium stone formers, making it the single most common metabolic abnormality in nephrolithiasis. ### Epidemiology of Stone-Forming Metabolic Disorders | Metabolic Disorder | Prevalence in Stone Formers | Stone Composition | Clinical Features | |---|---|---|---| | **Hypercalciuria** | 40–50% | Calcium oxalate/phosphate | Elevated 24-h urine calcium (>250 mg/day women, >300 mg/day men) | | Hyperoxaluria | 5–10% | Calcium oxalate | Primary (genetic) or secondary (GI disease, high dietary oxalate) | | Hyperuricemia | 5–10% | Uric acid or mixed | Gout history, elevated serum/urine uric acid | | Hypocitraturia | 20–30% | Calcium stones | Low urine citrate (<320 mg/day) | | Renal tubular acidosis | 1–2% | Calcium phosphate | Distal RTA, alkaline urine | ### Pathophysiology of Hypercalciuria 1. **Absorptive hypercalciuria** (most common subtype) — increased intestinal calcium absorption → increased urinary calcium 2. **Renal hypercalciuria** — reduced renal tubular reabsorption of calcium 3. **Resorptive hypercalciuria** — primary hyperparathyroidism (PTH-mediated bone resorption) **High-Yield:** In a patient with calcium oxalate stones and no systemic disease, hypercalciuria is the most likely diagnosis and should be confirmed by 24-hour urine calcium measurement. ### Clinical Pearl Hypercalciuria is often **asymptomatic** in its early stages and discovered only when stone formation occurs. It is the most common metabolic defect in both men and women with recurrent calcium nephrolithiasis. ### Management Approach - **First-line:** Dietary calcium restriction (not complete avoidance), increased hydration, and thiazide diuretics (reduce urinary calcium by 20–30%) - **Confirmation:** 24-hour urine calcium >250 mg/day (women) or >300 mg/day (men) on a normal diet - **Exclude:** Primary hyperparathyroidism (serum PTH, serum calcium) and vitamin D excess
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