Hemolysis is an important contributing cause of anemia in uremic patients. Uremia causes several erythrocyte abnormalities such as increased mechanical fragility1, increased autohemolysis2, and shortened erythrocyte survival1,2. These abnormalities may be due to a decrease in erythrocyte deformability, which is measured by filtrability as an index of cell rigidity. Several workers demonstrated that erythrocyte deformability is decreased in uremic patients3,4. Erythrocyte deformability is reduced by a rise in intracellular Na content, which may be due in part to a decline in the ATPase activity of the erythrocyte membrane. However, the relationship of erythrocyte deformability to uremic toxins has not been clarified. Giovannetti reported that guanidino compounds, especially methylguanidine (MG), caused hemolysis both in vivo and in vitro 5,6. Depressed Na-K ATPase activity of uremic erythrocytes was demonstrated by Cole7.
KeywordsATPase Activity Erythrocyte Membrane Standard Medium Uremic Patient Uremic Toxin
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