Allen R. Nissenson, MD; Stephen D. Nimer, MD; Deane L. Wolcott, MD
Anemia (hematocrit < 25%) predictably accompanies chronic renal failure and is present in over 90% of patients on chronic dialysis. Relative erythropoietin deficiency is the proximate cause. Recombinant human erythropoietin recently became available for research and clinical use. Erythropoietin production is regulated by a single copy gene located on chromosome 7; its expression has been shown in the kidney, liver, and macrophages. It is a glycosylated protein of 166 amino acids with a molecular weight of 34 000 D. When given to patients with the anemia of renal failure, erythropoietin causes a dose-dependent rise in hematocrit to the normal range within 8 to 14 weeks. Complications of this response are minimal except for a significant incidence of hypertension. When the anemia is corrected, the patient's quality of life, cognitive function, and brain electrophysiology improve dramatically. Recombinant human erythropoietin represents a major breakthrough in the treatment of patients with chronic renal failure. Current reimbursement constraints limit its full application.
Allen R. Nissenson, Stephen D. Nimer, Deane L. Wolcott. Recombinant Human Erythropoietin and Renal Anemia: Molecular Biology, Clinical Efficacy, and Nervous System Effects. Ann Intern Med. 1991;114:402–416. doi: 10.7326/0003-4819-114-5-402
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Published: Ann Intern Med. 1991;114(5):402-416.
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