The view that proteinuria in renal disease arises principally as a result of a reduction in the rate of renal tubular reabsorption of protein molecules, as opposed to the conventional belief in altered glomerular capillary permeability, rests upon the demonstration of a normal reabsorpfive mechanism and its disturbance in disease. Histologic evidence suggests that a variety of proteins may be abstracted from glomernlar filtrate in both normal and diseased kidneys (1) but there is little quantitative information concerning the rate at which this occurs. Moreover, physiologic evidence of protein reabsorption in normal circumstances is limited. For the protein hemoglobin a tubular transfer rate has been demonstrated (2), but the evidence of this for other proteins is for the most part inferential (1).Recently Eliasch and his associates (3) have demonstrated that the amino acid and polypeptide content of renal venous blood of normal rabbits exceeded that of arterial and vena caval blood. It was suggested that this difference might arise as a result of the renal tubular reabsorption, degradation, and metabolism of filtered protein. The present investigation was undertaken in order to examine this hypothesis in dogs. The free and total amino acid content of renal venous, arterial, and inferior vena caval blood was determined in fasting animals and following an infusion of hemoglobin, a protein for which there is considerable evidence of tubular reabsorption (2, 4). MethodFemale mongrel dogs, weighing between 7 and 30 kg., were anesthetized with sodium pentobarbital, 30 mg./kg, body weight, after a 24 hour fast. An indwelling needle was inserted into a femoral artery and a multiholed venous catheter was introducted into a jugular

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