par Naets, Jean-Pierre
Référence Nephron, 14, 2, page (181-194)
Publication Publié, 1975
Article révisé par les pairs
Résumé : Anemia is a frequent complication of renal failure. As in anemias of other origin, the resulting tissular hypoxia is partially compensated by an increased production of 2,3 diphosphoglycerate in red cells, and a shift to the right of the oxygen hemoglobin dissociation curve. Two mechanisms are implicated in this anemia: increased hemolysis, and depressed production of red cells. Decreased production of erythropoietin is probably the cause of reduced erythropoiesis, but the role of uremic intoxication has not been unequivocally excluded. In the course of chronic hemodialysis, iron deficiency anemia, and occasionally hypersplenism, develop. It is noteworthy that blood requirements in anephric patients are 2 to 3 times greater than those of nonanephric hemodialyzed patients. Accordingly, bilateral nephrectomy should be restricted to carefully selected cases. At the present time, androgens seem to be the best treatment of renal anemia. Qualitative anomalies of platelets are the main factor responsible for uremic bleeding, and are corrected by hemodialysis.