RENAL FUNCTION AND THE AZOTEMIA FOLLOWING HEMATEMESIS 1"2

Elevation of the blood urea nitrogen following massive hemorrhage from the stomach and duo-denum is a frequent occurrence (1). Its mecha-nism is not the same as that associated with high intestinal obstruction, as it occurs in the absence of any vomiting (2) (e.g. in the presence of melena alone4), and is associated with a normal or increased blood chloride concentration (3, 4, 5) and a normal carbon dioxide combining power of the blood (4, 5). The factors contributing to this increase of the urea nitrogen content of the blood have been said to comprise shock, de-hydration, starvation, renal insufficiency, and ab-sorption of decomposition products of the blood liberated in the intestinal tract. We have else-where adduced evidence which excludes the fac-tors of shock, dehydration, and starvation as es-sential but which emphasizes the importance of the digestion of the blood in the intestinal tract (1, 6). Attempts have previously been made to evalu-ate the renal factor in this increase of the blood urea nitrogen. Sanguinetti (7) found that three patients with elevated blood urea content follow-ing hematemesis were able to excrete a concen-ration of 30 to 38 grams of urea per liter of urine and believed that this excluded renal insufficiency. Christiansen (2) reported normnal kidneys at ne-cropsy in a case of hematemesis (due to peptic ulcer) in which there was an abnormally high blood urea concentration. Ingegno (8) empha-sized the presence of normal blood pressure, high urine specific gravity, and negative urinary find