PAX8 and Hypercalciuria: To confirm that deletion of Cldn2 causes hypercalciuria due to a functional transport defect and not due to a developmental abnormality, we generated inducible kidney-specific Cldn2-KO mice by crossing claudin-2 floxed mice to Pax8-LC1 (“Tet-On”) mice (Supplemental Figure 1; supplemental material available online with this article; https://doi.org/10.1172/JCI197807DS1).