Published online Jun 16, 2022. doi: 10.12998/wjcc.v10.i17.5893
Peer-review started: January 1, 2022
First decision: February 8, 2022
Revised: February 24, 2022
Accepted: April 4, 2022
Article in press: April 4, 2022
Published online: June 16, 2022
Processing time: 158 Days and 15 Hours
Gitelman syndrome (GS) is an autosomal recessive salt-losing renal tubulopathy arising from mutations in the thiazide-sensitive Na-Cl cotransporter gene. Due to its low incidence and lack of awareness, GS can be easily misdiagnosed or missed in diagnosis.
A 24-year-old male presented with > 4 years of repeated limb weakness without any treatment. The previous day, the patient was bitten by ants and showed weakness of the lower limbs. The patient had hypokalemia (1.66-2.83 mmol/L), hypomagnesemia (0.4 mmol/L), hypocalciuria (1.51-2.46 mmol/d), metabolic alkalosis (7.47-7.54), normal blood pressure, and increased activity of aldosterone and plasma renin activity (PRA) (PRA 6.4 and 16.45 ng/mL/h and aldosterone 330.64 and 756.82 pg/mL in the supine and upright position, respectively). In addition, SLCI2A3 gene mutation with GS was diagnosed. Oral and intravenous supplementation with potassium and magnesium was initiated. Serum magne
GS should be considered in patients with hypokalemia complicated with hypomagnesemia. Genetic testing is essential to confirm the diagnosis.
Core Tip: Gitelman syndrome (GS) is easily misdiagnosed or missed in diagnosis due to its low incidence and lack of awareness. Herein, we present a rare case of GS in a young man with limb weakness. This case demonstrates that attention should be focused on GS in patients with hypokalemia complicated with hypomagnesemia. Genetic testing is helpful in confirming the diagnosis.