Chloride channel 5 (CLC-5) mutations in apical endosomes in mouse models, as is also seen in Dent’s disease, demonstrate defective clathrin-mediated endocytosis and FPE, deficient endosomal acidification, internalization of the Na+-phosphate cotransporter 2 (NaPi-2) and NHE3, and increased proteinuria (226–228). The gene discussed is CLCN5; the disease is Dent disease.