Abstract
Since 1957, when Jacobson and associates1 demonstrated the renal origin of erythropoietin, it has been assumed that the anemia of chronic renal disease is caused at least in part by a deficiency of this renal hormone and that it might be corrected if erythropoietin could be administered in large enough quantities. Molecular biology has now provided such quantities, and Eschbach and associates, in this issue of the Journal,2 and Winearls and associates, in a recent issue of The Lancet,3 have provided convincing evidence for the therapeutic effectiveness of recombinant erythropoietin in anemic patients on long-term hemodialysis. This is . . .