Furosemide increases urinary acidification in control subjects and in certain patients with normokalemic or hypokalemic
distal renal tubular acidosis (RTA). We studied the effect of
furosemide in 14 patients with hyperkalemic distal RTA. In a group of patients with pure selective
aldosterone deficiency,
furosemide increased net
acid and K excretion in a fashion indistinguishable from controls. This effect of
furosemide was observed both in the presence and in the absence of acute
mineralocorticoid administration. In another group of patients with hyperkalemic distal RTA,
furosemide failed to decrease urine pH and to increase net
acid excretion despite acute
mineralocorticoid administration. Plasma
aldosterone was variable in this group in that some patients had appropriate levels of
aldosterone for the degree of
hyperkalemia, whereas in the other patients the levels were low. The failure of these patients to respond to
furosemide, despite pharmacologic doses of
mineralocorticoid, suggests that these patients had a defect in H+ secretion other than that attributable to
aldosterone deficiency alone. To gain insight into the mechanism whereby
furosemide increases urinary acidification, we studied control and
amiloride-treated rats pretreated with
mineralocorticoid. In response to
furosemide, control rats had a significantly lower urine pH and higher net
acid and K excretion than that observed in
amiloride-treated rats. These data suggest that
furosemide increases H+ and K excretion, at least in part, by creating a favorable electric gradient for secretion of these
ions since these effects were blunted in presence of inhibition of distal Na transport by
amiloride.(ABSTRACT TRUNCATED AT 250 WORDS)