Calcium moves through the tight junctions with water and sodium, and claudins 2, 10a, and 17 regulate this process.(53) Claudin 2, a cation‐selective isoform, has been shown to be particularly important for calcium homeostasis, as deletion in mice leads to a reduction in calcium reabsorption and increased delivery of calcium to the distal nephron, resulting in hypercalciuria and stone formation.(67) NHE3 on the apical membrane and Na/K ATPase on the basolateral membrane provide the driving force for passive transport (Fig. 2B). Here, CLDN2 is linked to Hypercalciuria.