INFECTIOUS complications in kidney transplant recipients are associated with significant morbidity and mortality. The risk of infection is based on two main factors: recent or past exposure to infectious agents, and the patient’s level of immunosuppression. Bacterial infections usually occur in the first month following transplantation, and technical issues related to the procedure can play an important etiologic role. Most febrile illness that occurs in kidney recipients between 1 and 6 months posttransplantation is caused by cytomegalovirus (CMV) and other opportunistic agents. The regimen and level of immunosuppression are important in the pathogenesis of these infectious complications. Kidney recipients whose grafts have come from cadavers tend to develop more frequent and severe infectious complications than living-donor kidney recipients due to the increased level of immunosuppression that is usually needed in the former group. Also, recipients of cadaveric kidneys who receive induction antilymphocyte globulin (ATG) preparations have higher infection rates than those who do not receive this treatment. Further, research has shown that patients who receive azathioprine as their primary immunosuppressive agent have a higher rate of infection than patients on cyclosporine-based regimens. Beyond 6 months, in patients with well-functioning allografts who are on stable maintenance immunosuppression the pattern of infection is similar to that in the general population. Another significant finding is that transplant recipients often develope infection that simultaneously involves several causal agents. This underlines the importance of considering concomitant infection in patients who do not respond to the initial line of treatment. While the incidence of tuberculosis (TB) after kidney transplantation in highly industrialized countries is low, the figure for developing regions is significantly higher. Mycobacterial disease should be considered in any patient with fever of unknown etiology. Most cases of Mycobacterium tuberculosis infection in kidney transplant recipients are due to reactivation of latent TB lesions. Important risk factors for reactivation include nonwhite race, history of active TB, presence of a marked abnormality on a chest radiograph, exposure to a person with a confirmed case of TB, and skin test positivity. In transplant patients, the clinical presentation of tuberculosis may be atypical, and extrapulmonary and miliary tuberculosis is seen more frequently than in the normal population. With regard to fungal infection, in kidney transplant recipients these most commonly present as prolonged fever that does not respond to antibiotic therapy. These infections are associated with very high mortality. The most common fungal infections reported in first series from developing countries were candidiasis, aspergillosis, and cryptococcosis. Several factors influence the development of symptomatic CMV infection after kidney transplantation, but most important are the CMV serologic statuses of the donor and recipient. Symptomatic CMV infection can be primary, can occur due to reactivation of latent infection, or can arise secondary to superinfection. The most severe form is usually observed when a CMV-seronegative recipient receives a graft from a CMV-seropositive donor. Host cell–mediated immunity and the type and level of immunosuppressive therapy influence the development of symptomatic CMV infections. Polyclonal and monoclonal antilymphocyte antibody treatments have the highest CMVpromoting effect, and represent the most important factor in the development of CMV infections after kidney transplantation. Nocardia is a filamentous gram-negative soil organism that can cause pneumonia. This infection also frequently disseminates to the brain and results in abscess formation. The overall mortality associated with nocardiosis in kidney transplant recipients is 25%, but this figure jumps to 44% in patients who have central nervous system involvement.
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