Infection and neoplasia are important complications of renal transplantation. Infection is common in the heavily immunosuppressed host (e.g., cadaveric transplant recipient with multiple episodes of rejection requiring steroid pulses or monoclonal antibody treatment). The culprit organism depends in part on characteristics of the donor and recipient and timing following transplantation (Table 141-3). In the first month, bacterial organisms predominate. After 1 month, there is a significant risk of systemic infection with cytomegalovirus (CMV), particularly in recipients without prior exposure whose donor was CMV positive. Prophylactic use of ganciclovir or valacyclovir can reduce the risk of CMV disease. Later on, there is a substantial risk of fungal and related infections, especially in pts who are unable to taper prednisone to <20-30 mg/d. Daily low-dose trimethoprim-sulfamethoxazole is effective at reducing the risk of Pneumocystis carinii infection.

The polyoma group of DNA viruses (BK, JC, SV40) can be activated by immunosuppression. Reactivation of BK is associated with a typical pattern of renal inflammation, BK nephropathy, which can lead to loss of the allograft; therapy typically involves reduction of immunosuppression to aid in clearance of the reactivated virus.

Epstein-Barr virus-associated lymphoproliferative disease is the most important neoplastic complication of renal transplantation, especially in pts who receive polyclonal (antilymphocyte globulin, used at some centers for induction of immunosuppression) or monoclonal antibody therapy. Non-Hodgkin's lymphoma and squamous cell carcinoma of the skin are also more common in this population.