Belatacept-based immunosuppressive therapy resulted in higher and more severe acute rejection compared with tacrolimus-based therapy. This trial did not identify cellular biomarkers predictive of rejection. In addition, the CD28-CD80/86 costimulatory pathway appeared to be sufficiently blocked by belatacept and did not predict rejection.

No abstract

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We analyzed the results of passive immunization against CMV in 146 heart transplant recipients. The 65 seronegative recipients were prophylactically treated with anti-CMV immunoglobulins during and after the operation. Twenty-nine of these 65 patients received a seropositive donor heart. CMV infection occurred in 21/65 seronegative and in 40/81 seropositive recipients (difference not significant). The incidence of CMV infection in seronegative recipients of a CMV-matched donor heart (3/34) was significantly lower than in seronegative recipients of a positive donor heart and lower than in seropositive recipients, but no significant difference in infection rate was found between the two latter groups (18/29 vs. 40/81). Although primary infection more frequently resulted in CMV disease than secondary infection (11/21 vs. 10/40) no difference in incidence of disease was noted between seronegative and seropositive patients (11/65 vs. 10/81), nor was there a difference in the severity of symptoms following primary or secondary infection. There was a higher incidence of CMV disease in all patients who received a heart from a seropositive donor versus a seronegative donor. However, after transplantation of a heart from a seropositive donor the incidence (27%) of CMV disease observed in our passively immunized seronegative patients was the same as in the patients with naturally acquired seropositivity. There was no difference in the prevalence of coronary artery disease between patients with and without CMV infection or disease. We conclude that using the current passive immunization scheme the occurrence of CMV infection and disease is largely dependent on the serostatus of the donor.

Cytomegalovirus (CMV) infections remain a major clinical problem after renal transplantation. Reported incidences of CMV disease range from 17 to 25% in patients with azathioprine treatment and from 2 to 23% in patients on cyclosporin A. CMV-related death occurs in 1-3% of the total kidney transplant population. CMV seronegative kidney recipients of a transplant from a seropositive donor are especially at risk for primary infection as CMV can be transmitted by the transplant. In patients treated with antilymphocyte globulin (ALG) preparations for rejection, CMV disease is diagnosed three to four times more frequent than in patients without ALG therapy. Prevention of CMV infection is possible by selecting CMV seronegative donors for seronegative recipients. Active and passive immunization does not prevent CMV infection after renal transplantation, but immunoprophylaxis may result in less severe CMV disease. Effective treatment of clinical overt CMV disease is possible with the new guanine analogue ganciclovir. However, the use of this drug is associated with neutropenia, especially in patients with compromised kidney function. More pharmacokinetic data are needed to determine optimal dosing schemes.