Background: Gitelman syndrome (GS) is an autosomal recessive, salt-losing tubulopathy caused by a defect in the thiazide-sensitive Na⁺-Cl⁻ cotransporter in the distal convoluted tubule. It presents with hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria. In resource-limited settings, diagnosis is often made on clinical and biochemical grounds without genetic confirmation. Objective: To describe the clinical and biochemical spectrum of six patients with GS diagnosed over two years at a tertiary care center. Methods: This case series included six patients diagnosed clinically and biochemically with GS between 2024 and 2025. Data on demographics, presenting symptoms, biochemical parameters, treatment, and outcomes over six months were collected at a tertiary care hospital in Dr. RPGMCT and a Himachal Pradesh, India. Genetic testing was not performed due to unavailability. Results: The mean age of patients was 39.7 ± 13.1 years (range 17–45 years), including 4 males and 2 females. One female had a history of hypertension; the rest had no co morbidities. All patients presented with generalized weakness, 5/6 had muscle cramps, 4/6 fatigue, and 3/6 paresthesias. Tetany was observed in 2 patients. Biochemical evaluation showed hypokalemia (2.50 ± 0.21 mEq/L), metabolic alkalosis (HCO₃⁻ 32 ± 1.41mEq/L),pH7.492 ± 0.016, hypomagnesemia (1.20 ± 0.14mg/dL), and hypocalciuria (urinary calcium 45 ± 18 mg/day). Plasma renin activity and aldosterone were elevated in all. Patients were treated with spironolactone, potassium, and magnesium supplements, resulting in symptomatic and biochemical improvement over six months, Conclusion: Recognition of the biochemical triad—hypokalemia, hypomagnesemia, and hypocalciuria-is crucial for diagnosis of Gitelman syndrome, even without genetic testing. Early identification prevents unnecessary investigations and complications. Gitelman syndrome (GS) is a rare autosomal recessive disorder affecting the thiazide-sensitive sodium-chloride co transporter (NCC),