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

Abstract

An abrupt and significant increase in the ammonia quantity released into the renal vein was observed in 11 patients with liver disease following the intravenous injection of 500 mg of acetazolamide. An equally rapid decrease in urine ammonia excretion and increase in urine pH was observed in 5 patients who had concomitant studies. The decrease in urine ammonia excretion approximated the increase in renal vein ammonia release. Arterial ammonia concentrations increased progressively during the 60 minute period of observation. These data demonstrate the role of the kidney in the pathogenesis of acetazolamide induced hyperammonemia and seem best explained by a shift in the partition of ammonia produced by the kidney between urine and renal vein. They also suggest that acute changes in the urine pH may also influence the amount of ammonia liberated into the renal vein.