CLDN16 and Hypercalciuria: Paracellular Ca2+ reabsorption is better characterized in the thick ascending limb, in which claudin-16 and claudin-19 form Ca2+ permeable pores and mutations in these genes cause the syndrome familial hypomagnesemia with hypercalciuria and nephrocalcinosis associated with severe renal Ca2+ wasting (16, 17).