The metabolism of copper and iron in the nephrotic syndrome has received little attention. In view of the fact that copper in the plasma is bound almost exclusively to an a2-globulin (ceruloplasmin) with a molecular weight of approximately 151,000 (1, 2) while iron is bound to a #l,-globulin (transferrin) with a molecular weight of about 90,000 (3), it would seem not unlikely that these two metal-binding proteins might be excreted in large quantities in the urine of patients with pronounced proteinuria. If this loss were great and extended over a prolonged period, it is conceivable that depletion of the body stores of these two elements might occur or the capacity of the body to synthesize these two proteins might be exceeded, with the consequence that the plasma level of ceruloplasmin and transferrin would be reduced.In the course of investigations in this laboratory concerning the anemia associated with infection (4), a patient was studied who, while afflicted with chronic osteomyelitis, developed the nephrotic syndrome. In association with the severe hypoproteinemia and proteinuria, the plasma copper level decreased from 246 ug. per 100 ml., the high levels usually found with infection, to 40 JUg. per 100 ml. in'spite of the continued presence of osteomyelitis. More recently (5) we observed hypocupremia in two of three children with the nephrotic syndrome. Munch-Petersen (6) has reported that the urinary excretion of copper is increased in patients with proteinuria and that the amount of copper excreted is greatest in those with the highest concentration of protein in the urine. Although he did not record the plasma copper values he stated that there was no correlation between the plasma copper concentration and the amount of copper in the urine.