Pretransplant recipient cytomegalovirus seropositivity and hemodialysis are associated with decreased renal allograft and patient survival.
BACKGROUND
Pretransplant systemic inflammation has been associated with decreased renal allograft survival, and infectious agents such as cytomegalovirus (CMV) may play a role. We hypothesized that pretransplant CMV seropositivity is a risk factor for decreased patient and allograft survival after cadaveric renal transplantation and that other factors believed to modulate systemic inflammation, such as dialysis modality, might act synergistically with CMV to decrease patient and allograft survival.


METHODS
The United Network for Organ Sharing database was reviewed to identify all patients undergoing cadaveric renal transplantation in the United States from 1988 to 1997. Outcomes for CMV seropositive and seronegative recipients of organs from CMV seronegative donors were analyzed. Subgroup analysis was performed to identify any synergistic influence on outcome between CMV serostatus and known determinants of risk, including degree of human leukocyte antigen mismatch, pretransplant dialysis, and cold ischemia time.


RESULTS
Of 29,875 patients who underwent transplantation, 12,239 were CMV seronegative and 17,636 were CMV seropositive. Patient survival was decreased by pretransplant seropositivity (relative risk [RR] 1.11, P =0.001). In addition, this group demonstrated worse overall allograft survival (RR 1.05, P =0.029), although this adverse effect disappeared when patients who died with a functioning graft were censored. Decreased allograft survival was most pronounced in patients who were on hemodialysis before transplantation (RR 1.62, P =0.004).


CONCLUSIONS
Pretransplant CMV seropositivity is associated with decreased patient survival. Pretransplant CMV seropositivity and hemodialysis have a synergistic adverse effect on graft survival, independent of patient mortality. Additional studies are required to define mechanisms by which pretransplant CMV infection and dialysis modality may contribute to decreased allograft survival.
Fitzgerald
Jason T
JT
Department of Surgery, Division of Transplantation, University of California, Davis Medical Center, Sacramento, California 95817, USA. hellfitz@aol.com
Gallay
Brian
B
Taranto
Sarah E
SE
McVicar
John P
JP
Troppmann
Christoph
C
Chen
Xiaowu
X
McIntosh
Matthew J
MJ
Perez
Richard V
RV
D000208:Acute Disease; D000328:Adult; D000914:Antibodies, Viral / Q000097:blood; D002908:Chronic Disease; D003080:Cold Temperature; D003586:Cytomegalovirus Infections / Q000276:immunology / Q000401:mortality*; D005260:Female; D006085:Graft Survival; D006680:HLA Antigens / Q000276:immunology; D006801:Humans; D007511:Ischemia / Q000401:mortality; D007676:Kidney Failure, Chronic / Q000401:mortality* / Q000601:surgery / Q000628:therapy; D016030:Kidney Transplantation / Q000276:immunology / Q000401:mortality*; D008297:Male; D006435:Renal Dialysis / Q000401:mortality*; D012307:Risk Factors; D016019:Survival Analysis; D013997:Time Factors; D014184:Transplantation, Homologous; D016896:Treatment Outcome
D000914:Antibodies, Viral; D006680:HLA Antigens