role of sialic acid in the development of anemia in chronic renal failure

ABSTRACT

Shortened life span of erythrocytes has been suggested as one of the causes of anemia in chronic renal failure. Decreased sialic acid content of erythrocytes lead to their rapid removal from the circulation. Abnormalities in metabolism of this substance with increased neuraminidase activity in sera of these patients may be responsible for this phenomenon. To clarify this hypothesis, sera of 50 patients with end stage renal failure were examined before and after dialysis for neuraminidase activity by assessing their effect on desialylation of erythrocytes of healthy subjects, matched for blood group and of fetuin [substrate rich in sialic acid] together with determination of total and lipid bound sialic acid content of their RBCs. The results were compared with corresponding values of 20 controls. The study showed a significantly enhanced neuraminidase like activity in sera of patients with chronic renal failure in comparison with sera of healthy controls [P<0.001] associated with significant decrease of total and lipid bound sialic acid of RBCs. The present data are indicating that increased neuraminidase activity in sera of patients with chronic renal failure could be a contributing factor involved in the mechanism of producing the marked anemia in uremic subjects by acting on erythrocytes, rendering them more liable to be cleared faster by the liver and spleen, shortening their life span, moreover, it could act on erythropoietin depriving it from its sialic acid content, shortening its life span therefore reevaluation of the therapeutic modalities of anemia in these patients whether blood transfusion or erythropoietin is needed