In addition, the lowering of intracellular Na+ concentration facilitates Ca2+ exit via a basolateral Na+/Ca2+ exchanger [11] Defective basolateral Cl− exit in the DCT decreases NaCl reabsorption via the NCC, accounting for the GLS phenotype, including hypocalciuria in BS type III patients with impaired ClC-Kb function in the DCT [4].Accordingly, II-3 has isosthenuria and a significantly elevated uCa/Cr ratio, which both indicate the tubular location of the CLCNKB mutation was in the TAL instead of DCT. Here, SLC12A3 is linked to Hypocalciuria.