Polyoma viral infection in renal transplantation: the role of immunosuppressive therapy.
BACKGROUND
Polyoma virus infection in renal transplant recipients has been observed with increasing frequency in recent years. Renal allograft involvement in this condition may occur as a result of primary infection or secondary to reactivation of the latent virus. Interstitial nephritis, ureteric stenosis, rise in serum creatinine and allograft function loss have been attributed to this viral infection.


METHODS
In this study we reviewed our experience with 8 patients who developed polyoma viral infection confirmed by allograft biopsy. All patients were receiving mycophenolate mofetil as part of the immunosuppression and 7 of the 8 patients were on tacrolimus. All patients have biopsy proven polyoma viral infection. The following therapeutic maneuvers were carried out following the diagnosis of polyoma viral infection: 1) stopping mycophenolate and 2) switching tacrolimus to cyclosporine or reducing the tacrolimus dose to adjust it at a lower therapeutic trough level. The clinical course and outcome of our patients were reviewed in relation to manipulation of immunosuppressive medications.


RESULTS
The incidence of this infection in our transplant program in the last 3 yr was 5.3%. Seventy-five percent of the patients had at least one rejection episode and 63% had more than one rejection episode. The main risk factor for the development of polyoma viral infection was related to the intensity of immunosuppression. The use of antirejection therapy after histological diagnosis of polyoma virus infection was not associated with improvement of renal function despite the histological appearance of acute rejection. Thus, the interstitial nephritis associated with polyoma viral infection appears to be an inflammatory response to the virus rather than acute rejection. Six out of the 8 patients stabilized renal function with reduction in immunosuppression.


CONCLUSIONS
Reduction in immunosuppression was associated with the stabilization of renal function when instituted early. However, these patients were left with a degree of allograft dysfunction and their outcome may be significantly compromised. The lack of effective antiviral therapy for polyoma virus may limit the use of newer and more potent immunosuppressive medications.
Barri
Y M
YM
Division of Nephrology, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare Services, Little Rock, AR 72205, USA. barriyousri@exchange.uams.edu
Ahmad
I
I
Ketel
B L
BL
Barone
G W
GW
Walker
P D
PD
Bonsib
S M
SM
Abul-Ezz
S R
SR
D000208:Acute Disease; D000328:Adult; D016572:Cyclosporine / Q000009:adverse effects*; D005260:Female; D006084:Graft Rejection / Q000517:prevention & control / Q000821:virology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects*; D007668:Kidney / Q000473:pathology; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D009173:Mycophenolic Acid / Q000009:adverse effects / Q000031:analogs & derivatives*; D009395:Nephritis, Interstitial / Q000209:etiology* / Q000473:pathology / Q000821:virology; D027601:Polyomavirus Infections / Q000209:etiology* / Q000473:pathology; D012307:Risk Factors; D016559:Tacrolimus / Q000009:adverse effects*; D014412:Tumor Virus Infections / Q000209:etiology* / Q000473:pathology
D007166:Immunosuppressive Agents; D016572:Cyclosporine; D009173:Mycophenolic Acid; D016559:Tacrolimus