THE PATHOGENESIS OF ANEMIA IN ACUTE GLOMERULONEPHRITIS. ESTIMATIONS OF BLOOD PRODUCTION AND BLOOD DESTRUCTION IN A CASE RECEIVING MASSIVE TRANSFUSIONS

1. A 27 year old patient with an initial episode of acute glomerulonephritis was observed over a fifty day period, studies being directed primarily in an attempt to define the mechanisms responsible for a rapidly developing anemia. Hematologic data, including serial blood volume measurements and selective agglutination counts were obtained before and after the introduction of massive transfusion therapy.

2. The administration of group-O whole blood containing incompatible anti-A isoagglutinins in the first series of transfusions failed to improve the anemia but initiated a sustained reticulocyte response. Following this therapy there was evidence of increased blood destruction involving both the recipient’s and the normal donor erythrocytes.

3. Data obtained following a second series of transfusions employing plasma-free group-O red cells, administered during a recovery phase when renal function had improved, indicated that blood destruction had largely abated and that hemopoietic activity was normal.

4. Two factors of undetermined origin are believed to have been implicated in the pathogenesis of anemia in this case: one, the occurrence of abnormally rapid blood destruction, and the other, impairment of blood formation. Both phenomena were associated with the presence of nitrogen retention, despite which, however, a prompt erythropoietic response followed the transfusion of whole blood with quantitative replacement of patient’s red cells with donor erythrocytes, suggesting that previous bone marrow inactivity was not attributable to "toxic suppression."