Figure 138

The course of normal erythropoiesis after renal transplantation showing mean serum erythropoietin levels of 31 recipients [14]. An initial burst of erythropoietin (EPO) secretion at the time of engraftment does not result in erythropoiesis. As excellent graft function is achieved, a second burst of EPO secretion is normally followed by effective production of erythrocytes. The hatched area is the range of serum erythropoietin levels in normal persons without anemia.

Anemia is a common complication. Many patients leave the dialysis population with diminished iron stores and are unable to respond to erythropoietin produced by the successful allograft. Iron replacement therapy successfully restores erythropoiesis in these patients. Another common cause of anemia after transplantation is bone marrow suppression owing to drug therapy with azathioprine or mycophenolate mofetil (MMF), an effect that is usually dose-related [15,16]. Other drugs, notably angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists, may also inhibit erythropoiesis [17].

Neutropenia also is a common complication after transplantation. It can reflect dose-related bone marrow suppression owing to drug therapy with azathioprine or MMF or an idiosyncratic response to a number of drugs commonly used in this population (acyclovir, ganci-clovir, sulfa-trimethoprim, H2 blockers). Alternatively, neutropenia can be a manifestation of systemic viral, fungal, or tubercular infections. The approach to the patient with neutropenia usually involves reducing the dose or discontinuing the potential offending agents, along with a careful search for infections. In some settings of refractory neutropenia, administration of filgrastim (granulocyte colony-stimulating factor, Neupogen®) reduces the duration and severity of neutropenia. (From Sun and coworkers [14]; with permission.)

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