Bartter's syndrome is clinically important in the differential diagnosis of hypokalemia associated with inappropriate kaliuresis in adults. In children, short stature and failure to thrive represent manifesting clinical features. The syndrome classically is defined by the combined presence of hypokalemic alkalosis, inappropriate kaliuresis, hyperaldosteronism, hyperreninemia, and overproduction of renal prostaglandins (PGs) (PGE and prostacyclin) in the setting of normal BP and relative vascular resistance to the pressor effects of angiotensin II and norepinephrine.1-3 Histologic examination of renal tissue typically discloses hyperplasia of the juxtaglomerular apparatus.1
Despite the seemingly explicit nature of this constellation of biochemical abnormalities, functional vascular derangements, and histopathologic changes, no precise or unique pathogenesis for this syndrome has been delineated with certainty. The most recent pathogenetic clue derives from the demonstration of defective reabsorption of chloride ions in the loop of Henle.2 Notably, neither hypokalemia nor the defect in chloride reabsorption is corrected by
Veldhuis JD. The Many Faces of Hypokalemia. Arch Intern Med. 1983;143(8):1521–1522. doi:10.1001/archinte.1983.00350080027005
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