title: Why the kidney?
abstract: Severe erythrocytosis is associated with increased whole blood viscosity and impaired blood flow. Since a reduced blood flow will cause tissue hypoxia and since tissue hypoxia is associated with increased synthesis of erythropoietin, erythrocytosis per se should cause an increase in the rate of red cell production. This, however, does not occur and severe erythrocytosis in patients with polycythemia vera does not lead to increased synthesis of erythropoietin. We propose here that the reason for this discrepancy is that decreased blood flow to the kidneys, the site of erythropoietin synthesis, does not cause renal tissue hypoxia. The oxygen tension in the kidneys is to a great extent determined by the consumption of oxygen used for sodium reabsorption and since sodium reabsorption is roughly proportional to glomerular filtration, a decreased flow of blood should be matched by a decreased oxygen consumption leaving the tissue tension of oxygen unchanged. Consequently, the location of an oxygen sensor in the kidneys controlling erythropoietin production appears to be most fortuitous since it prevents the development of a vicious circle, with erythrocytosis causing more erythrocytosis.
mesh_terms: D001809:Blood Viscosity; D004921:Erythropoietin / Q000096:biosynthesis; D005919:Glomerular Filtration Rate; D006400:Hematocrit; D006801:Humans; D000860:Hypoxia; D007668:Kidney / Q000098:blood supply*; D010101:Oxygen Consumption; D011086:Polycythemia / Q000150:complications / Q000503:physiopathology*; D011087:Polycythemia Vera / Q000150:complications; D011863:Radioimmunoassay; D012039:Regional Blood Flow; D012964:Sodium / Q000378:metabolism
chemical_list: D004921:Erythropoietin; D012964:Sodium