Hypercalciuria, defined as the urinary excretion of more than 0.1 mmol Ca/kg/d (4 mg/kg/24 h), is observed in approximately 50% of patients with calcium oxalatelapatite nephrolithiasis and is one of the risk factors for stone formation. Urinary Ca excretion rates among such patients are higher than normal, despite comparable ranges of glomerular filtration rate (GFR) and serum ultrafiltrable Ca concentrations, and thus glomerular filtration of Ca, suggesting that hypercalciuria is the result of inhibition of net tubular Ca reabsorption. Although increased dietary NaCl or protein intake and reduced K intake increase urinary Ca excretion rates, urinary Ca excretion rates are higher among hypercalciuric stone formers than among normal subjects in relation to comparable ranges of urinary Na, SO₄ (as a reflection of protein intake), or K excretion rates, indicating that these dietary factors are not primarily responsible for hypercalciuria. Hypophosphatemia is observed among a subset of hypercalciuric patients and consequent activation of 1,25-(OH)₂-D synthesis increases intestinal Ca absorption and urinary calcium excretion. Other hypercalciuric patients exhibit augmented intestinal Ca absorption without elevated plasma 1,25(OH)₂-D levels, suggesting that either the capacity of 1,25-(OH)₂-D to upregulate its own receptor in the intestine or 1,25-(OH)₂-D-independent intestinal Ca transport are responsible for increased Ca absorption and hypercalciuria. Hypercalciuric patients also exhibit accelerated radiocalcium turnover, negative Ca balances, reduced bone density, delayed bone mineralization, fasting hypercalciuria, and increased hydroxyproline excretion, all of which reflect participation of the skeleton and presumably a more generalized acceleration of Ca transport. Hypercalciuria may be familial. Recent studies have shown that urinary Ca excretion rates among normal subjects and patients with stones, without or with hypercalciuria, is directly related to the activity of Ca-Mg-adenosine triphosphatase (ATPase) in erythrocytes. Since this enzyme is present in the distal renal tubule, alteration in its activity may contribute to hypercalciuria. Hypercalciuria thus appears to reflect a spectrum of disorders, mainly of genetic origin, that have not yet been precisely defined.