Anemia in the kidney-transplant patient

Anemia, a potentially correctable cardiovascular risk factor, continues to be a major problem in kidney-transplant patients. Erythropoietin levels increase rapidly after successful kidney transplantation, and by 3 months, most patients achieve hemoglobin levels greater than 12 g/dL. Anemia may be caused by problems commonly seen in the general population such as iron deficiency or gastrointestinal blood loss, by immunosuppressive medications, or by more rare abnormalities such as hemolytic uremic syndrome or parvovirus B19-induced aplastic anemia. Iron deficiency is common at the time of transplantation and beyond and frequently contributes to anemia. Markers of iron deficiency (ferritin or transferrin saturation) are frequently inconclusive because of the presence of inflammation and infection. Immunosuppressive medications, such as azathioprine and mycophenolate mofetil (MMF), are a common cause of mild bone-marrow suppression and, thus, anemia. Sirolimus can cause more severe bone-marrow suppression, although this effect can lessen over time. The transplant patient with chronic kidney disease (CKD) frequently develops anemia, yet agents such as epoetin-α and darbepoetin are greatly underutilized. Evaluation of anemia should be undertaken when hemoglobin fails to normalize by 3 months after transplantation. Later after transplantation, especially in the setting of chronic allograft dysfunction, evaluation should take place when the hemoglobin falls to less than 11 g/dL in premenopausal females or to less than 12 g/dL in males and postmenopausal females.