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

Abstract

The role of the gastrointestinal tract as a major source of blood ammonia has been extensively studied in animals and in patients with liver dis-ease. Less information is available concerning the relative contribution to the blood ammonia by other organs, such as muscle, liver, brain and kid-ney, which are known to be concerned with am-monia metabolism (1). The renal release of am-monia 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 investiga-tion. 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 sug-gest that total renal ammonia production may re-main unchanged following acute alterations in urine pH (9). Of particular interest in this re-gard have been the observations of significant in-creases in arterial ammonia concentrations of cir-rhotic 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 empha-sis on the effect of intravenous acetazolamide. METHODS Eleven patients with liver disease were studied. All were hospitalized males, ranging in age from 32 to 63 * This investigation was supported (in part) by a re-