Monocyte-macrophage mediated suppression of erythropoiesis in renal anaemia.

To investigate monocyte-macrophages and their secretions in the pathogenesis of renal anaemia we studied the following in 12 uraemic patients and in 12 normal subjects: 1. in vitro proliferation of erythroid progenitors (BFU-e) from uraemic and normal peripheral whole mononuclear cells; 2. effects of monocyte-depletion of uraemic or normal whole mononuclear cells on proliferation of BFU-e; 3. effects of adding uraemic or normal peritoneal macrophages (PM0) to peripheral blood normal non-adherent mononuclear cells; and 4. Interleukin-1 (IL-1) and prostaglandin E2 (PGE2) concentrations in supernatants of uraemic and normal PM0. BFU-e growth from uraemic whole mononuclear cells is lower than that of normal whole mononuclear cells. The removal of monocytes induces an increase in BFU-e development in uraemic patients, but a decrease in normal subjects. The addition of uraemic PM0 to normal nonadherent mononuclear cells causes a decrease in BFU-e formation, compared to values incubating normal PM0. PGE2 release in supernatants of uraemic PM0 is greater than in supernatants of normal PM0, and IL-1 activity is less with uraemic PM0 than that with normal PM0. In Conclusion we found that uraemic monocyte-macrophages have a suppressive effect on BFU-e development in vitro which can be mediated by abnormal release of secretory products.