The appearance of proteinuria in patients suffering from congestive heart failure is a common clinical occurrence. Since such patients, without any intrinsic renal disease, frequently have both an elevated renal venous pressure and a reduced renal blood flow (1), it would seem that either one or both of these factors may lead to proteinuria.Proteinuria has been produced experimentally by partial obstruction either of the renal artery or of the renal vein (2-5). In most of this work, however, studies of renal hemodynamics were incomplete, or when adequate pressure and blood flow measurements were made (6, 7), the experiments were such that it was impossible to determine specifically which hemodynamic factor was responsible for the appearance of the proteinuria.The present study was The estimations of renal plasma flow (RPF) and glomerular filtration rate (GFR) for each kidney were made by determining the clearances of para-aminohippurate (PAH) and exogenous creatinine, respectively. Blood samples were drawn at the midpoint of each clearance period from the right femoral artery through an indwelling needle. During the operative procedure the animal was given intravenously a priming d.nse of 1.5 grams of creatinine dissolved in 30 ml. of water. This was followed by a sustaining infusion of an 0.85 per cent NaCl solution delivered at a constant rate of 3 or 5 ml. per minute by a Bowman Pump for the remainder of the experiment. This sustaining infusion contained sufficient amoants of creatinine and PAH so that these substances were delivered at rates of 20 mg. of creatinine per minute and 3 mg. of PAH per minute. In some instances an additional infusion of NaCl solution (0.85 or 1.5 per cent) was given during the course of the experiment. The reason for this will be discussed later.After completion of the operative procedure the animal was allowed to recover for about 30 minutes. One or more control urine samples were then collected in order to measure the clearances and determine the presence of proteinuria. The clamp was then tightened until the pressure in the left renal vein rose to the desired level. After the pressure had been elevated for 15 to 30 minutes, con-secutive urine samples were collected until proteinuria appeared or until the pressure had been elevated for 1 to approximately 3 hours without the occurrence of proteinuria. The clamp was then released allowing the pressure in the left renal vein to fall freely.After an interval of time at least sufficient to allow the renal dead space to be cleared, one or more recovery samples were collected.Creatinine concentration in urine and plasma was determined by the method of Kennedy, Hilton, and Berliner (9). PAH concentration in urine and plasma was determined by the method of Smith, Finkelstein, Aliminosa, Crawford, and Graber (10).The method used to determine the concentration of protein in urine was a modification of the method of 737

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In the anesthetized dog the pCO2 of the urine, arterial blood, and renal venous blood was measured before and after the intravenous administration of Diamox (acetazoleamide). The pCO2 of the urine always rose to a much greater degree than did the pCO2 of the arterial or renal venous blood This rise in urinary pCO2 could be explained satisfactorily neither by a rise in intracellular pCO2 nor by an increase in the rate of urine flow, but seemed best explained by the fact that Diamox itself acted as a urinary buffer.