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October 23, 1987


JAMA. 1987;258(16):2256-2258. doi:10.1001/jama.1987.03400160110027

The translation of new insights derived from fundamental research to the field of clinical nephrology is occurring at an increasing pace. Two recent developments directly stem from the revolution in biomedical science brought about by the remarkable tools of molecular biology. The first was cloning, in 1984, the gene responsible for the production of human erythropoietin,1,2 followed by its insertion into a mammalian cell-line vector, allowing large-scale synthesis of the pure harmone.3

Erythropoietin is a 166—amino acid polypeptide with molecular weight of 34 000 daltons, which is secreted as a glycosolated product.4 The anemia that accompanies chronic renal failure is primarily due to the kidneys' diminished synthesis and production of erythropoietin, which results in reduced bone-marrow red blood cell production. Shortened red blood cell survival, blood loss, intoxications such as lead or aluminum, and associated nutritional deficiencies may aggravate the anemia.5

Two clinical trials using recombinant human