Pathogenesis of the anemia of uremia: role of secondary hyperparathyroidism.
PTH may participate in the genesis of the anemia of uremia through at least three pathways. These include inhibition of erythropoiesis, shortening survival of RBCs and inducing fibrosis of bone marrow cavity. A possible fourth mechanism through which PTH may contribute to the anemia of uremia is its effect on platelets. PTH inhibits platelet aggregation [53] and, as such, may play an important role in the genesis of the bleeding tendencies and the consequent blood loss in uremia.
D000740:Anemia / Q000209:etiology*; D000747:Anemia, Hypochromic / Q000209:etiology; D000756:Anemia, Sideroblastic / Q000209:etiology; D000818:Animals; D003114:Colony-Forming Units Assay; D004905:Erythrocyte Aging; D004920:Erythropoiesis; D004921:Erythropoietin / Q000172:deficiency; D005494:Folic Acid Deficiency / Q000097:blood; D006412:Hematopoietic Stem Cells / Q000473:pathology; D006461:Hemolysis; D006470:Hemorrhage / Q000097:blood; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000097:blood* / Q000209:etiology; D066298:In Vitro Techniques; D051379:Mice; D010281:Parathyroid Hormone / Q000097:blood; D014511:Uremia / Q000097:blood*
D010281:Parathyroid Hormone; D004921:Erythropoietin