Erythropoietin Alterations in Renoprival and Renal Allografted Patients

Mirand, E. A.; Murphy, G.P.; Steeves, Richard A.; Groenewald, J. H.; Zyl, J. J. W. Van; Retief, F. P.

doi:10.3181/00379727-129-33434

Cited by 3 publications

(9 citation statements)

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“…Whereas erythropoiesis has been observed in man and animals with renal lesions (Mirand, 1968a), anemia was seen in acute and chronic renal insufficiency (Tables I11 and IV). The mechanism of anemia of uremia in acute and chronic renal insufficiency results from various factors.…”

Section: Discussionmentioning

confidence: 99%

“…Abnormal renal function is usually associated with alterations in ESF titers and erythropoiesis (Mann et al, 1965;Mirand, 1968a;Kurtides et al, 1965;Joske et al, 1956;Kaye, 1958). Whereas erythropoiesis has been observed in man and animals with renal lesions (Mirand, 1968a), anemia was seen in acute and chronic renal insufficiency (Tables I11 and IV).…”

Section: Discussionmentioning

confidence: 99%

“…Plasmas were collected from each group of tamarins and assayed for E S F activity in polycythemic mice (Mirand, 1968a).…”

Section: Tamarinsmentioning

confidence: 99%

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The effects of uremia on erythropoietin activity

Mirand

Murphy

1969

Journal of Surgical Oncology

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Erythropoietin (ESF) activity was determined during acute and chronic uremic states with and without evidence of excretory renal function in humans. These observations demonstrated that detectable endogenous levels of ESF were absent in humans during an acute and chronic uremic state. Unlike the humans, the experimental animals produced ESF at a diminished rate. Also, in experimental animals, factors appear by 48-60 hr which make the bone marrow and spleen less responsive t o exogenous ESF. Therefore, the human and nonhuman data show that the anemia of the uremic state can be explained by two factors: (1) an initial inhibition of end-organ ESF responsiveness, and (2) a failure in ESF production. The temporal difference in the effect of these two aspects of erythropoietin activity is perhaps the basis for the variability in measured ESF activity in acute and chronic uremic states.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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The effects of uremia on erythropoietin activity

Mirand

Murphy

1969

Journal of Surgical Oncology

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“…Recently 19-ND has been reported to be a strong erythropoietic stimulant in mice [20] and in man [3], The mechanism by which ESF production is stimulated by androgens is not clear. Hypoxic exposure can stimulate ESF production even in a nephrectomized state [2,14,35,43], Tissue hypoxia [41] or hypoxic ex posure [40] may be compensated for by a 'right shift' of the oxygen disso ciation curve [41] along with an increase of RBC 2,3-DPG. Hyperoxia exerts a suppressive effect on the ESF level [22,31] and has also been re ported to suppress the RBC 2,3-DPG level [25].…”

Section: Discussionmentioning

confidence: 99%

“…Hyperoxia has abolished detectable rising levels of plasma ESF and RBC 2,3-DPG following androgen administration. These levels were close to those seen in the ambient nontreated mice.The erythropoietic capacity of androgens has long been recognized [13,16,35]. It has been clearly demonstrated [1,13] that androgens are capable of stimulating erythropoietin (ESF) production.…”

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confidence: 99%

Effect of Hyperoxia and Androgen on Red Cell 2,3-Diphosphoglycerate and Oxygen Affinity

Gorshein¹,

Gardner²,

Tyree³

et al. 1976

Acta Haematol

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Increased plasma erythropoietin (ESF) activity, a rise in RBC 2,3-DPG, and a ‘right shift’ of the oxygen hemoglobin equilibrium curve following androgen administration to mice in ambient or hyperoxic conditions, was demonstrated. If androgens had a direct effect on the RBC metabolism, increased 2,3-DPG would result in a facilitated release of oxygen to the tissue. This would have been accompanied by a decrease rather than an increase in the level of ESF. Hyperoxia has abolished detectable rising levels of plasma ESF and RBC 2,3-DPG following androgen administration. These levels were close to those seen in the ambient nontreated mice.

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