Recombinant human erythropoietin and renal anemia: molecular biology, clinical efficacy, and nervous system effects.
Anemia (hematocrit less than 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 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.
Nissenson
A R
AR
Department of Medicine, UCLA School of Medicine.
Nimer
S D
SD
Wolcott
D L
DL
D000740:Anemia / Q000188:drug therapy* / Q000209:etiology; D000818:Animals; D004921:Erythropoietin / Q000235:genetics / Q000378:metabolism / Q000502:physiology / Q000627:therapeutic use*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000378:metabolism / Q000523:psychology; D011994:Recombinant Proteins / Q000627:therapeutic use; D006435:Renal Dialysis / Q000523:psychology
D011994:Recombinant Proteins; D004921:Erythropoietin