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Eugene P. Frenkel, MD; Charles C. Douglass, MD; Mary Sue McCall

Arch Intern Med. 1970;125(6):1050-1055.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Aprime aspect of the anemia associated with renal disease is the evidence of a hypoproliferative state, in essence an erythron which appears to lack erythropoietic stimulus. That the erythropoietic stimulus is a humoral material (erythropoietin) with its origin or activation in the kidney was first demonstrated by Jacobson and co-workers in 1957.^1,2 Recent reviews by Gordon et al,³ Adamson et al,⁴ and Stohlman ⁵ have documented the extensive investigative data clarifying the important role of the kidney in man as a primary site of erythropoietin production and its resultant action in the regulation of red blood (RBC) production. Although extrarenal erythropoietic stimulatory potential appears to exist in man,^6-11 the renal source or renal activation of erythropoietin is the presumed physiologically significant mechanism in the normal modulation of erythropoiesis. Characteristic of the nonstimulated or hypoproliferative anemia of renal disease is that the degree of the anemia is . . . [Full Text PDF of this Article]

Author Affiliations
Dallas

From the Department of Internal Medicine, University of Texas Southwestern Medical School, and the Radioisotope Laboratory, Veterans Administration Hospital, Dallas. Dr. Douglass is now at the Clinic of the Southwest, Houston.

Footnotes
Received for publication Nov 21, 1969; accepted Feb 2, 1970.

Reprint requests to 5323 Harry Hines Blvd, Dallas 75235 (Dr. Frenkel).

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