In hypoaldosteronemic patients with
chronic renal insufficiency, administration of a
mineralocorticoid steroid such as
fludrocortisone can ameliorate
hyperkalemia and
metabolic acidosis, but this
therapy is not always safe owing to the deleterious consequences of extracellular fluid volume expansion resulting from
mineralocorticoid-induced
sodium chloride retention. In the present study of 8 patients with renal hyperchloremic
acidosis, mild
hyperkalemia and chronic glomerular insufficiency, we evaluated the
therapeutic effect of chronic administration of a natriuretic/chloruretic agent,
furosemide, a renoactive
drug that is known to increase renal
acid excretion in experimental animals without increasing body content of
sodium chloride. 4 patients had
hyporeninemic hypoaldosteronism. During 8 days of treatment in 6 patients who received
furosemide alone,
metabolic acidosis was significantly ameliorated. Urinary net
acid excretion increased, except in the 2 patients who had the most severe
hypoaldosteronism. For the group as a whole, the cumulative change in net
acid excretion correlated positively with the rate of
aldosterone excretion (r = 0.94, p less than 0.01). Thus, the aciduric response to
furosemide is attenuated by
aldosterone deficiency. When
furosemide was administered in combination with
fludrocortisone (4 subjects), an amelioration of
metabolic acidosis occurred that was greater than that observed in the group treated with
furosemide alone. Combined
therapy ameliorated
acidosis in the patient with the most severe degree of
hypoaldosteronism, the same patient in whom administration of
furosemide without
fludrocortisone was ineffective even after 6 months of treatment. The findings in this study indicate that chronic
furosemide therapy, alone or in combination with
fludrocortisone, is a safe and effective means of ameliorating
metabolic acidosis in patients with
chronic renal insufficiency, including those with
hypoaldosteronism.