ANEMIA Anemia in ESRD patients is of multifactorial origin, secondary to decreased erythropoietin, blood loss from dialysis, and decreased red blood cell survival times. In addition, wide fluctuations in plasma blood volume seen in dialysis patients often cause factitious anemia. Without treatment, the hematocrit in ESRD patients will usually stabilize at 15 to 20 percent, with normocytic and normochromic red blood cells. Bone marrow will show erythroid hypoplasia with little effect on leukopoiesis or megakaryocytopoiesis. Management of anemia is by the infusion of human recombinant erythropoietin on a regular basis. Erythropoietin replacement therapy has markedly improved the quality of life for ESRD patients by increasing exercise capacity and tolerance. An increase in blood pressure has been reported in approximately 30 to 35 percent of patients receiving erythropoietin.
BLEEDING DYSCRASIA Abnormalities in hemostasis expose ESRD patients to increased risks of GI tract bleeding, subdural hematomas, subcapsular liver hematomas, and intraocular bleeding. The abnormal hemostasis in ESRD is characterized by decreased platelet function and von Willebrand factor defects. 9 Anemia has been determined to be the major etiologic defect causing abnormal hemostasis in ESRD patients. The skin bleeding test is the best predictor of clinically important defects in hemostasis. Improvements in bleeding times can be obtained by infusion of desmopressin, conjugated estrogens, and erythropoietin.
NEUTROPHIL DYSFUNCTION Immunologic deficiency in ESRD patients produces a high mortality rate from infectious diseases. Both leukocyte chemotaxis and phagocytosis are depressed in uremic patients. Abnormal T-cell activation has also been noted in ESRD patients secondary to reduction in interleukin 2 production. Dialysis therapy does not appear to improve the immune function of leukocytes or T cells. In fact, HD may even exacerbate immunodeficiency by complement activation after exposure to the HD filter membrane.
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