A shortened life of erythrocytes in uremia has been suggested as one of the causes of anemia in this condition. Since partially desialylated erythrocytes are promptly removed from the circulation, we examined whether sera from renal failure patients would exhibit increased neuraminidase activity which could be held responsible for this phenomenon. Sera of 22 patients with end stage renal failure were examined for neuraminidase activity by assessing their effect on desialylation upon incubation at 37°C for 2 and 1 h, respectively, of erythrocytes of healthy donors matched for blood group and of fetuin as substrate. As deduced from the residual content of sialic acid of erythrocytes and of the amount of sialic acid released from fetuin, the results showed a statistically higher neuraminidase-like activity of patients' sera as compared to sera of healthy individuals. It is suggested that increase in neuraminidase activity could be one of the factors involved in he mechanism of generation of anemia in uremia by acting on erythrocytes, rendering them more prone to sequestration by the liver and spleen.