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The role of the gastrointestinal tract as a major source of blood ammonia has been extensively studied in animals and in patients with liver disease. Less information is available concerning the relative contribution to the blood ammonia by other organs, such as muscle, liver, brain and kidney, which are known to be concerned with ammonia metabolism (1). The renal release of ammonia into the systemic circulation was first demonstrated by the observations of Nash and Benedict in 1921 (2). Although the magnitude of this ammonia release and its effect on the arterial ammonia concentration have not been determined, factors affecting the quantity of ammonia excreted into urine have engendered considerable investigation. Current evidence indicates that changes in urine pH are important determinants of urinary ammonia excretion, lesser amounts of ammonia appearing in alkaline than in acid urines (3-8). Studies in unilaterally nephrectomized dogs suggest that total renal ammonia production may remain unchanged following acute alterations in urine pH (9). Of particular interest in this regard have been the observations of significant increases in arterial ammonia concentrations of cirrhotic patients given Diamox (acetazolamide) (10-12), an agent which is known to increase urine pH. The present investigation is concerned with the release of ammonia into the renal vein of patients with liver disease, with particular emphasis on the effect of intravenous acetazolamide.

THE KIDNEY AS A SOURCE OF BLOOD AMMONIA IN PATIENTS WITH LIVER DISEASE: THE EFFECT OF ACETAZOLAMIDE *†