ADH1 accounts for ∼70% of ADH cases9 and has a biochemical phenotype opposite of FHH1, i.e., individuals have low serum Ca concentrations, normal or low PTH concentrations, relative or absolute hypercalciuria, and may have symptomatic hypocalcemia and ectopic calcifications affecting the kidneys and/or basal ganglia.8 This evidence concerns the gene ADH1A and Hypocalcemia.