Graves’ hyperthyroidism is a clinical syndrome characterized by increased excitability of the nervous, circulatory, and digestive systems, electrolyte disturbances such as hypokalemia, calcium and phosphorus, and hypermetabolism. The syndrome is characterized by autosomal renal disease. Hyperthyroid periodic paralysis is a common cause of hyperkalemia in Graves’ hyperthyroidism, but Gitelman syndrome should be considered if potassium does not increase after potassium supplementation. Hypokalemia is the primary symptom of both hyperthyroid cyclic paralysis and Gitelman syndrome. The difference between the two is that hypokalemia is transient in patients with hyperthyroid cyclic paralysis and that thyroid hormones stimulate bone cells, promoting bone turnover and increased urinary calcium. Hypocalciuria is usually seen in patients with Gitelman syndrome, so refractory hypokalemia, hypocalciuria, hypomagnesemia, and activation of the renin-angiotensin system should be considered first for the diagnosis of Gitelman syndrome. SLA12A3 is considered the causative gene for GS, and genetic testing is the gold standard for GS diagnosis; peripheral blood genetic testing identified mutations in the SLC12A3 gene (G → C, glycine → alanine). In general, patients with Gitelman syndrome without obvious clinical symptoms are generally not considered for drug treatment; potassium (oral potassium chloride, etc.), magnesium, potassium-protective diuretics, and NSAIDs are given for obvious symptoms, and magnesium supplementation is more important than potassium supplementation, and if there is no efficacy, then administration of anisotropic therapy is considered.