CLINICAL STUDIES IN ACIDOSIS AND ALKALOSIS; USE AND ABUSE OF ALKALI IN STATES OF BICARBONATE DEFICIENCY DUE TO RENAL ACIDOSIS AND SULFANILAMIDE ALKALOSIS

Abstract

Plasma BHCO3 reduction in chronic nephritis and other forms of renal insufficiency may occur with the production of a real acidosis of the "metabolic type" without abnormal acid retention, due fundamentally to inadequate reabsorption by the tubules of BHCO3 from the glomerular filtrate. Severe and persistent acidosis was noted in an infant of 4 mos. in whom the only clearly demonstrable renal lesion seemed to be failure of the tubules to reabsorb BHCO3. There is a logical use for the adm. of alkali, particularly as Na r-lactate, in such cases, both to relieve and prevent recurrence of significant degrees of acidosis. Plasma BHCO3 reduction, which follows sulfanilamide adm., must be looked upon as compensatory for a primary CO2 deficit alkalosis. There is no logical use for the routine use of alkali with sulfanilamide to "prevent acidosis.".