Hypokalemia and Prostaglandin Overproduction in Bartter’s Syndrome

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Abstract
In 2 adult patients with Bartter''s syndrome, in whom Cl reabsorption at the diluting segment of the nephron was markedly reduced, serum K concentration could be improved with oral administration of a large amount of KCl. In both cases, improvement of serum K levels with oral K load resulted in an increase in plasma renin activity (PRA) and plasma aldosterone concentration (PAC), a decrease in urinary excretion of prostaglandin E2 (PGE2) and prostaglandin F2.alpha. (PGF2.alpha.), and an improvement of pressor responsiveness to angiotensin II and norepinephrine. Treatment with indomethacin also improved the pressor responsiveness to angiotensin II and norepinephrine, but this occurred in association with a decrease in PRA, PAC and urinary excretion of PGE2 and PGF2.alpha.. Apparently, an event at the renal tubular level leading to K depletion is the most proximal pathogenetic defect in Bartter''s syndrome, and that this in turn contributes to excessive prostaglandin production leading further to the decreased pressor responsiveness to vasoactive substances.