This report describes the case of a 50-year-old male with end-stage renal failure accompanied with congenital heart disease and polycythemia. After he had received continuous ambulatory peritoneal dialysis for 1 year, he still remained polycythemic and his serum erythropoietin titer, assayed using fetal mouse liver cells, was markedly increased. An inhibitory effect on erythropoiesis was not detected by this method. Bone marrow examination showed erythroid hyperplasia. These phenomena could be explained by an overproduction of erythropoietin by the remnant kidneys or extrarenal organs, such as the liver, in response to persisting hypoxia. The patient’s bone marrow was still responsive to erythropoietin.

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