FGF23 and familial hypocalciuric hypercalcemia: Our findings highlight the importance of increased serum calcium concentrations arising from attenuated CaSR signal transduction, altered vitamin D homeostasis, and increased urinary phosphate excretion via effects on FGF23, 1-α hydroxylase, and 24 hydroxylase in the pathogenesis of common idiopathic forms of KSD as well as in the rare monogenic kidney stone–associated diseases FHH, IH1, and IH2, respectively.