A biological phenotype of Bartter syndrome has also been reported in different damages of molecular structures that directly or indirectly affect sodium reabsorption in the Henle loop: the calcium-sensing receptor (CaSR, activating mutation L125P) that mainly leads to hypocalcemia and hypercalciuria, sometimes referred as type V Bartter syndrome [6], the Chloride channel-5 (ClC5) [7], and the cystinosin [8]. The gene discussed is CLCN5; the disease is Hypercalciuria.