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Bartter syndrome is a rare autosomal recessive primary salt-losing tubulopathy characterized by defective sodium and chloride reabsorption in the thick ascending limb of the loop of Henle. The resulting urinary salt loss leads to hypokalemic, hypochloremic metabolic alkalosis and secondary hyperaldosteronism. Despite elevated renin and aldosterone, blood pressure remains normal because of increased prostaglandin and bradykinin activity. Based on the gene defect and age of onset, Bartter syndrome is classified as antenatal or classic forms, with further subdivision into five molecular types. Early identification and prompt management are crucial to prevent chronic kidney disease, growth retardation, and recurrent dehydration, especially in children from consanguineous families.
This retrospective case series analyzed six pediatric patients diagnosed with Bartter syndrome at our tertiary care center over a five-year period. Clinical history, anthropometric data, biochemical parameters, imaging findings, and genetic studies were reviewed. Each patient was evaluated for presenting symptoms, complications, therapeutic response, and follow-up outcomes. Genetic confirmation was obtained through clinical exome sequencing
The study included six children, aged between 3 months and 15 years. Four were boys and 2 were girl children. Three were antenatal Bartter syndrome with a history of polyhydramnios and preterm birth, three represented classic Bartter syndrome with later onset. The predominant clinical manifestations were polyuria, polydipsia, vomiting, dehydration, and faltering of growth. All children demonstrated hypokalemia and metabolic alkalosis, with elevated renin and aldosterone levels. One adolescent male showed bilateral medullary nephrocalcinosis and was genetically confirmed to have Bartter syndrome type II due to a homozygous KCNJ1 mutation. Mortality was 50% (3 children) due to acute gastroenteritis in 2 and multi organ dysfunction syndrome in one child. Treatment consisted of potassium chloride supplementation, prostaglandin synthesis inhibitors (Indomethacin), and potassium-sparing diuretics (Spironolactone). All 3 children showed improvement in hydration status, biochemical stability, and symptom control, though significant growth lag persisted in those with severe early-onset disease.
Bartter syndrome presents a wide clinical spectrum ranging from antenatal detection with polyhydramnios to childhood-onset with growth retardation and metabolic disturbances. Early recognition, correction of electrolyte abnormalities, and genetic confirmation are essential for improving outcomes. A multidisciplinary management approach involving nephrology, nutrition, and genetics can minimize complications and enhance long-term prognosis. Lifelong follow-up is vital to monitor renal function and prevent progression to chronic kidney disease.
Table 1: Case series
