The Action and Neutralization of a Renal Lipid Inhibitor of Erythropoietin

Erslev, Allan J.; Kazal, Louis A.; Miller, Orin P.

doi:10.3181/00379727-138-36043

Cited by 10 publications

(2 citation statements)

References 4 publications

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“…They suggested still a third hypothesis to explain why biologically active EP can be obtained from kidney extracts only after mixing them with plasma or serum. These investigators [32,35] showed that when partially purified EP is incubated with a lipid soluble material extracted from the kidneys, its biological effect is inhibited. However, if the EP is mixed with plasma prior to or immediately after incubation with the renal lipid, the biological activity of the EP is restored.…”

Section: Role O F the Kidneys In Production Of Erythropoietinmentioning

confidence: 99%

Erythropoietm and the Kidney

Fried¹

1975

Nephron

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Erythropoietin is a polypeptide hormone, which is produced in response to a deficit in the delivery of oxygen to the tissues relative to their oxygen needs; although other feedback mechanisms also modulate its production. The kidneys play a major role in the elaboration of this hormone. However, the precise action of the kidney is not yet known. Diseases of the kidneys cause profound alteration in the normal regulation of erythropoiesis. Some of these are reviewed here.

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Section: Role O F the Kidneys In Production Of Erythropoietinmentioning

confidence: 99%

Erythropoietm and the Kidney

Fried¹

1975

Nephron

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“…The plasmatic substrate has not yet been identified. On the other hand, an inhibitor of erythropoietin has been demonstrated in kidney homogenates [24,36] and has been extracted recently from the kidney by Erslev et al [26] as a lipidic substance. We have shown recently that the kidney is necessary for normal catabolism of the hormone and that the T/2 of erythropoietin is increased in nephrectomized rats [78], This finding is not surprising, as other proteins such as insulin [15], Pa-microglobulin [4], and Bence-Jones protein [105] are likewise catabolized by the kidney.…”

Section: Erythropoietinmentioning

confidence: 99%

Hematologic Disorders in Renal Failure

Naets¹

1975

Nephron

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Anemia is a frequent complication of renal failure. As in anemias of other origin, the resulting tissular hypoxia is partially compensated by an increased production of 2,3-diphosphoglycerate in red cells and a shift to the right of the oxygen hemoglobin dissociation curve. Two mechanisms are implicated in this anemia: increased hemolysis and depressed production of red cells. Decreased production of erythropoietin is probably the cause of reduced erythropoiesis, but the role of uremic intoxication has not been unequivocally excluded. In the course of chronic hemodialysis, iron deficiency anemia and occasionally hypersplenism develop. It is noteworthy that blood requirements in anephric patients are two to three times greater than those of nonanephric hemodialyzed patients. Accordingly, bilateral nephrectomy should be restricted to carefully selected cases. At the present time, androgens seem to be the best treatment of renal anemia. Qualitative anomalies of platelets are the main factor responsible for uremic bleeding and are corrected by hemodialysis.

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The Reticuloendothelial System and Erythropoiesis

Naughton

Gordon

1984

Physiology

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The Action and Neutralization of a Renal Lipid Inhibitor of Erythropoietin

Cited by 10 publications

References 4 publications

Erythropoietm and the Kidney

Erythropoietm and the Kidney

Hematologic Disorders in Renal Failure

The Reticuloendothelial System and Erythropoiesis

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