Abstract: Gitelman syndrome (GS), also known as familial hypokalemia and hypomagnesemia, is a hypokalemic renal tubular disease caused by mutation in gene encoding the renal thiazide-sensitive sodium-chloride cotransporter (NCC), which is expressed in the distal convoluted tubule (DCT). GS is characterized by hypokalemic alkalosis and hypomagnesemia. At present, the main pathogenic genes of GS are SLC12A3 gene, KCNJ10 gene, HNF1B gene and so on. Gitelman-like syndrome has the same clinical manifestation as GS, but no classic gene mutation. It has not exactly the same pathogenic mechanism as GS. This paper summarizes the pathogenesis of Gitelman-like syndrome from genetic factors (mitochondrial gene variation, SLC26A4 gene mutation, BSND gene mutation, etc.) and non-genetic factors (diuretic abuse, aminoglycosamine antibiotics, cisplatin, etc.), in order to provide theoretical basis for further understanding, diagnosis and treatment of the disease.