The effect of acute alkalosis on renal metabolism of ammonia in cirrhotics.

The kidney consistently releases ammonia into the renal venous circulation of normal subjects and patients with compensated liver disease (1-4). Under conditions of normal acid-base balance, the quantity released usually approximates the amount of ammonia excreted into urine (3, 4). From determinations of arteriovenous ammonia differences across various organs, it has become apparent that the release of ammonia into the renal vein represents a major source of the normal ammonia concentration in blood (5). Of possible clinical importance in this regard is the observation that under certain conditions patients with liver disease may increase their renal contribution of ammonia to the systemic circulation. The increase of blood ammonia concentration seen after the intravenous administration of acetazolamide and chlorothiazide can be adequately explained by concomitant increases in release of ammonia into renal vein (3, 6). It has been suggested that the alterations in renal ammonia release seen during carbonic anhydrase inhibition may result from a shift in the normal partition of ammonia between urine and renal venous blood because of a disproportionate increase in pH of urine as compared with that of peritubular fluid (3). The present study deals with acute metabolic and respiratory alkalosis and was designed to obtain additional information on the role of the kidney in the regulation of the ammonia concentration in blood and to evaluate the effects of acute systemic alkalosis on total bidirectional renal release of ammonia.