Patricia Kaye B. Regalado
Gitelman’s syndrome (GS) is an inherited benign salt-losing tubulopathy characterized by hypokalemic metabolic alkalosis, hypomagnesemia and hypocalciuria and is often diagnosed in adolescents and middle-aged population. GS features include electrolyte imbalance, symptoms such as severe fatigue, cramps, polyuria and nocturia, and hypertension. Asymptomatic GS have also been reported and would present as an incidental finding.
Gitelman condition (GS) is an autosomal latent kidney tubule issue portrayed by low blood levels of potassium and magnesium, diminished discharge of calcium in the pee, and raised blood pH.[2] The confusion is brought about by hereditary transformations bringing about ill-advised capacity of the thiazide-touchy sodium-chloride symporter (otherwise called NCC, NCCT, or TSC) situated in the distal tangled tubule of the kidney.[2] The distal tangled tubule of the kidney serves a negligible job in salt ingestion and a more prominent job in dealing with the discharge of electrolytes like magnesium and calcium to deliver increasingly focused urine.[3]
PDFShare this article