Abstract
In chronic glomerulonephritis usually there is a progressive normocyte anemia which becomes manifest as renal insufficiency progresses and increases with the elevation of nitrogen retention. 1 There is, furthermore, no apparent lack of active blood-forming tissue, nor has there been any evidence presented to suggest that blood loss or increased hemolysis may play a rôle. 1 2
With the progress of renal insufficiency in glomerulonephritis there is an accretion of various chemical constituents in the blood plasma. The increase of certain of these, namely, urea and indican, is generally accepted, and certain studies on the blood phenol indicate that this substance likewise is increased. 3 It occurred to us that these retained substances in particular may play a rôle in the anemia of nephritis, and that they may cause hemolysis of such a degree as is not detectable by the ordinary tests usually employed for the determination of increased fragility.
Herrald and Pijoan 4 investigating the behavior of erythrocytes in a hemolytic system using standardized saponin as the lytic agent, demonstrated that the red cells of nephritic patients are more resistant than those of normal subjects to saponin hemolysis. However, they were unable to offer any adequate explanation for this phenomenon. Suspecting that indican, phenol and urea might play a rôle in hemolysis, we decided to investigate this problem using the method described by Herrald and Pijoan. Our plan was to compare the saponin hemolysis curves of the red cells of uremic patients with red cells from normal subjects, and then to add proportionally the same amounts in their equivalent proportion of urea, indican and phenol to red cells of normal subjects with and without saponin.
Red cells from uremic patients with the exception of those in the extreme terminal stage were found to hemolyze more slowly in saponin systems than normal cells, which is in agreement with the previous study. 4
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