Hypercalcemia-induced hypokalemia has been well-documented in BBM patients, with the phenomenon attributed to renal mechanisms involving activation of calcium-sensing receptors in the thick ascending limb, which suppress sodium–potassium–chloride cotransporter activity and promote kaliuresis, while concurrent volume contraction stimulates aldosterone release and further exacerbates potassium loss [59,60,61]. Here, CASR is linked to hypercalcemia disease.