The renal phenotypes seen in patients with ADKH-RRAGD resemble Bartter syndrome and familial hypomagnesemia, hypercalciuria, and nephrocalcinosis, in which the TAL section of the renal tubule is affected.32, 33, 34, 35 In family 9, which is affected by the variant, p.(Thr97Pro), the absence of hypercalciuria and nephrocalcinosis more closely resembles Gitelman syndrome, where the Na+-Cl− cotransporter is impaired, suggesting a defect in the distal convoluted tubule.36 Here, SLC12A3 is linked to Gitelman syndrome.