CYP24A1 and idiopathic hypercalciuria: This subgroup may well represent a physiologically distinct subpopulation within our ISF cohort, i.e., individuals with latent idiopathic hypercalciuria, the mechanism for which might be genetic (e.g., a CYP24A1 mutation or polymorphism [28] leading to intrinsic hypersensitivity to vitD as a consequence of hampered degradation of 1,25-(OH) vitD by 1,25-(OH)2 vitD hydroxylase: genotyping such patients for CYP24A1 would be a reasonable next step to consider.