HEMATOPOIESIS IN RENAL-FAILURE PATIENTS

Although the complex relationship between the kidney and hematopoiesis is still not yet entirely clear, the literature of the last 10 years has allowed certain physiological and pathophysiological aspects to be defined. Chronic renal failure anemia is due to an insufficient release of erythropoietin (EPO), which may be consequent to a down regulation of O2 sensors. The immunosuppressive state of chronic uremic patients is partly connected with a functional defect of monocytes and T-and B-lymphocytes, and partly with a fall in the bone marrow reserve and production of granulocytes, consumption of which is increased in patients on RDT. Hemorrhage in uremic patients is partly accounted for by a diminished mean platelet life-span, by a reduction in the circulating platelet mass and a defect in the activity of these cells owing to inadequate functioning of the glycoprotein adhesion receptors. Dialysis treatment corrects, but does not normalize, the hemorrhage syndrome. Anemia can now be corrected by rHu-EPO, and, in emergency situations or where there is risk of infection, the production and function of granulocytes can be stimulated by rHu-G-CSF. Transplant solves the hematologic problem but subjects the patient to a state of chronic immunodepression.