The hypercalciuria observed in patients with Dent's disease and some ClC-5-deficient mice may be secondary to the PT dysfunction (urinary loss of vitamin D binding protein and reduced phosphate absorption, leading to increased 1,25(OH)2-vitamin D3 synthesis) or, at least in part, caused by the functional loss of ClC-5 in the TAL. Here, CLCN5 is linked to Hypercalciuria.