The anemia of chronic renal failure. Studies of iron transport in vitro.
Many studies indicate that serum from patients with CRF contains a material(s) which inhibits erythropoiesis in vitro. Little is known concerning the nature or mechanism of action of this inhibitory substance. Previous work has shown that 59Fe-heme synthesis rates of normal human or animal erythroblasts were suppressed in the presence of CRF serum. To further study the mechanism of inhibition of CRF serum, we evaluated the amount of iron present in various cellular fractions as a function of time in a fluid marrow culture system. Our data show that a reduction in heme synthesis occurs in plates prepared with uremic serum, which becomes most marked after 24 hr in culture. We were unable to find any significant difference in the amount of 59Fe attached to cellular membranes or in cell cytosol in cultures prepared with either normal or CRF serum. The data reject the hypothesis that the inhibitor somehow interferes with erythroblast membrane iron receptors or transport but suggest that it exerts its effort on heme synthesis.
D000328:Adult; D000740:Anemia / Q000209:etiology / Q000378:metabolism*; D001692:Biological Transport; D002463:Cell Membrane Permeability; D004920:Erythropoiesis; D005260:Female; D006418:Heme / Q000096:biosynthesis; D006801:Humans; D007501:Iron / Q000378:metabolism*; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D008875:Middle Aged
D006418:Heme; D007501:Iron