Recombinant human erythropoietin and renal anemia: Molecular biology, clinical efficacy, and nervous system effects

Allen R. Nissenson, Stephen D. Nimer, Deane L. Wolcott

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)402-416
Number of pages15
JournalAnnals of internal medicine
Volume114
Issue number5
DOIs
StatePublished - Mar 1 1991
Externally publishedYes

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ASJC Scopus subject areas

  • Internal Medicine

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