Inhibitors of erythroid colony-forming cells (CFU-E and BFU-E) in sera of azotemic patients with anemia of renal disease.
A number of potentially toxic compounds accumulate in the sera of patients with end-stage renal disease, and some have been demonstrated to inhibit erythropoiesis. In vitro CFU-E and BFU-E erythroid colony growth was compared in the presence of sera from patients with anemia of renal insufficiency and normal human subjects with the use of plasma clot cultures of normal rabbit bone marrows. In studies of sera from nine undialyzed patients with anemia of renal insufficiency and seven normal human subjects, all undialyzed sera from the anemic uremic patients produced a significant (p less than 0.001) inhibition of both CFU-E and BFU-E. A marked reduction in the inhibitor of CFU-E was seen in the sera of three out of four patients following intermittent hemodialysis. Creatinine, guanidine hydrochloride, guanidinosuccinic acid, and guanidinobutyric acid did not affect the number of CFU-E in normal rabbit bone marrow cultures. These data suggest that uremic toxins in the sera of undialyzed anemic uremic patients inhibit erythropoiesis, are partially removed by regular hemodialysis, and may play an important role in the mechanism of the anemia associated with renal insufficiency. These inhibitors of CFU-E do not appear to be creatinine or guanidine derivatives.[1]References
- Inhibitors of erythroid colony-forming cells (CFU-E and BFU-E) in sera of azotemic patients with anemia of renal disease. Ohno, Y., Rege, A.B., Fisher, J.W., Barona, J. J. Lab. Clin. Med. (1978) [Pubmed]
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