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Much of the disability induced by chronic Bright's disease, particularly during the nephrotic stage, is attributable to thte coexistent disturbances in protein metabolism. The latter may be characterized as follows: 1, proteinuria; 2, hypoalbuminemia; and 3, depletion of tissue protein stores. During the past few years, numerous attempts have been made to correct the hypoalbuminemia, depletion of body protein stores, and attendant edema in patients with nephrotic syndromes by administering human plasma intravenously (1, 2, 3). This form of therapy obviously had as its objectives the use of protein solution as a diuretic agent by virtue of its high colloid osmotic pressure, the restoration of serum albumin level, and the replenishment of body protein stores. The last two objectives were rarely, if ever, attained because of the limited quantity and high cost of human

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