Hypercalciuria is the most common metabolic abnormality that causes urolithiasis. The pathogenetic mechanisms responsible for hypercalciuria include enhanced gastrointestinal absorption of calcium, increased bone resorption and/or decreased renal reabsorption of calcium; the main dietary factors promoting hypercalciuria are high dietary sodium intake and protein-rich diet. The authors discuss pathophysiology of hypercalciuria and genetic factors behind 'idiopathic hypercalciuria'. The simplified diagnostic approach to hypercalciuria is outlined herein, and available therapeutic interventions of proven efficacy in idiopathic hypercalciuria are presented as well. Dietary intervention for hypercalciuria should include reduced sodium, protein and oxalate intake. Thiazide diuretics, in conjunction with a low-sodium diet, tend to reduce urinary calcium excretion and ameliorate idiopathic hypercalciuria. Potassium citrate acts as an inhibitor of calcium stone formation in the urinary tract. A low-calcium diet should generally be avoided, as it may increase urinary oxalate excretion and actually promote stone formation. In addition, a low-calcium diet may lead to negative calcium balance in subjects with hypercalciuria, and therefore increases the risk of osteopenia.