AMMONIA AS A SOURCE OF GASTRIC HYPOACIDITY IN PATIENTS WITH UREMIA *

Abstract
As compared to 24 control subjects without evidence of renal dysfunction, 26 patients with uremia had significantly higher gastric ammonia and lower free and total acid concentrations, both in basal and posthistamine secretion (p<0.05). Mean ammonia concentrations of basal and posthistamine gastric secretions were lowered significantly (p < 0.05) in uremic and non-uremic subjects treated by oxytetracycline (20 mg/kg) given orally for 4-7 days and gastric juice urea concentration rose to a similar extent. Chloramphenicol and erythromycin had variable effects. In all the control subjects and in patients with uremia where no marked reduction of gastric ammonia was measured, no significant change of acidity was observed; while in 8 patients with uremia in whom antibiotics resulted in a significant drop of gastric ammonia, a significant increase of gastric acidity (p<0.05) occurred which reached a level similar to that of non-uremic subjects. The parallelism between the falll of gastric ammonia and the rise of acidity indicates the contribution of ammonia to hypoacidity in uremia.