CMV infection of the renal allograft is much more common than the pathology indicates: a retrospective analysis of qualitative and quantitative buffy coat CMV-PCR, renal biopsy pathology and tissue CMV-PCR

Liapis, Helen; Storch, Gregory A.; Hill, D. Ashley; Rueda, Jose; Brennan, Daniel C.

doi:10.1093/ndt/18.2.397

Cited by 46 publications

(34 citation statements)

References 12 publications

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“…Furthermore, viral load would have been higher [31] if it had not been for the high number of patients who received prophylaxis with ganciclovir. This agrees with the findings of other authors [20,[28][29][30]; however, the overlap of symptomatic and asymptomatic patients is too great and just the opposite conclusion should be drawn. Further studies should be conducted in order to validate the cut-off values obtained by quantitative PCR in this study.…”

Section: Evaluation Of the Diagnostic Assays For Detection Of CMV Infsupporting

confidence: 91%

Significance of nested PCR and quantitative real time PCR for cytomegalovirus detection in renal transplant recipients

Kanaan

Cour

Álvarez‐Lafuente

et al. 2004

International Journal of Antimicrobial Agents

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Section: Evaluation Of the Diagnostic Assays For Detection Of CMV Infsupporting

confidence: 91%

Significance of nested PCR and quantitative real time PCR for cytomegalovirus detection in renal transplant recipients

Kanaan

Cour

Álvarez‐Lafuente

et al. 2004

International Journal of Antimicrobial Agents

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“…However, CMV viremia itself was not significantly different among the five groups in this study (P=0.80) ( Table 1). There may be a unique interaction of these two DNA viruses that is both common in renal transplant recipients and displays tropism for kidney tissue (15).…”

Section: Discussionmentioning

confidence: 99%

Transient versus Persistent BK Viremia and Long-Term Outcomes after Kidney and Kidney–Pancreas Transplantation

Elfadawy

Flechner

Schold

et al. 2014

Clinical Journal of the American Society of Nephrology

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Background and objectives The objective was to study the long-term impact of transient versus persistent BK viremia on kidney transplant outcomes.Design, setting, participants, & measurements In total, 609 recipients who underwent kidney transplant from 2007 to 2011 were screened at months 1-12 for the occurrence of polyomavirus BK viremia; 130 patients (21.7%) developed BK viremia during the first year post-transplant. BK viremia patients were classified according to duration of infection (more or less than 3 months), and BK viral loads (more or less than 10,000 copies/ml) were classified as transient low viremia (n=42), transient high viremia (n=18), persistent low viremia (n=23), and persistent high viremia (n=47). All patients were followed a median of 36 (3-66) months. The rates of BK polyomavirus-associated nephropathy, acute rejection, and 1-year graft function were compared with the polyomavirus BK-negative control group.Results Patient and graft survival were not significantly different among the groups. Graft function (creatinine; milligrams per deciliter) at 1 year was significantly worse in the persistent high viremia (1.7560.6) and transient high viremia (1.8560.7) groups compared with aviremic controls (1.4760.4; P=0.01 and P=0.01, respectively). The incidence of BK polyomavirus-associated nephropathy was limited to the persistent high viremia group (1.3%, P,0.001). The transient high viremia (50%) and persistent high viremia (34%) groups showed significantly (P=0.01) increased incidence of acute rejection versus aviremic controls (21.5%), transient low viremia (19%), or persistent low viremia (17.3%) groups.Conclusion Low viral load BK viremia, either transient or persistent, was not associated with long-term transplant outcomes. Persistent high viremia was associated with a greater risk for BK polyomavirus-associated nephropathy and subsequent graft dysfunction. Although transient high viremia was not associated with BK polyomavirus-associated nephropathy, it was associated with worse graft function. These data support the role of surveillance for BK viremia after transplant.

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“…Several possibilities include CD4+ T cell immunity, natural killer cells, and humoral immunity. However, sensitive DNA-based techniques commonly detect CMV persistence after transplantation in kidneys from seropositive donors, 24 suggesting that donor tissue may act as a "reservoir" for infection, which may later become clinically manifest. 25 Certainly the preimplantation histologic data from the current study suggest peri-transplantation CMV transmission is very common.…”

Section: Discussionmentioning

confidence: 99%

“…The endpoint for this investigation was the development of CMV replication (irrespective of the development of symptomatic disease) within the first 12 months after transplantation. Serial whole-blood samples were taken for CMV DNA PCR in these patients at day 0 (before transplantation) and then at weeks 1, 2, 3, 4,6,8,10,12,16,20,24,28,34,40, 46, and 52. This cohort of patients were contained within the larger "retrospective" cohort described above.…”

Section: Predicting Post-transplant CMV Infection By Pretransplant Asmentioning

confidence: 99%

Impaired Direct Priming of CD8 T Cells by Donor-Derived Cytomegalovirus Following Kidney Transplantation

Shabir

Kaul

Pachnio

et al. 2013

Journal of the American Society of Nephrology

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Cytomegalovirus (CMV) infection increases the risk of complications after renal transplantation, but the mechanisms controlling donor-derived infection are not adequately characterized. Here, we assessed the risk of clinically significant CMV disease in donor-seropositive, recipient-seropositive (D+R+) renal transplantation and examined recipients' CMV antigen-specific cellular immune responses primed directly by donor cells. In a retrospective cohort of 569 patients administered standardized basiliximab-tacrolimus-mycophenolate-corticosteroid immunosuppressive therapy, CMV disease rates increased in D+R+ serostatus pairings compared with D2R+ pairings (hazard ratio [HR], 2.61; 95% confidence interval [CI], 1.36 to 5.01; P=0.004) and associated with increased donor-recipient HLA mismatch in the D+R+ group (HR [per class 1 mismatch], 1.43; 95% CI, 1.12 to 1.82]; P=0.02). D+R+ and D+R2 transplants in which the donor and recipient differentially expressed at least one HLA class I allele were followed prospectively from the time of transplantation. During the first year after transplantation, four of eight seropositive recipients and one of three seronegative recipients displayed peripheral blood CD8+ T cell responses to CMV presented by recipient-specific HLA. Notably, no recipients mounted responses to CMV presented by donorspecific HLA, despite the detection of CMV antigen expression in all seropositive donor organs examined (n=10), suggesting that the allograft of Class I HLA-mismatched seropositive donors is inaccessible to CD8+ T cell responses. Finally, pretransplant assays of anti-CMV cellular immunity predicted post-transplant CMV replication less accurately in D+R+ pairings than in D2R+ pairings, possibly reflecting in vitro assay specificity for recipient, rather than donor, HLA. These findings are relevant to the clinical management and immunologic understanding of donortransmitted viral infection.

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CMV infection of the renal allograft is much more common than the pathology indicates: a retrospective analysis of qualitative and quantitative buffy coat CMV-PCR, renal biopsy pathology and tissue CMV-PCR

Cited by 46 publications

References 12 publications

Significance of nested PCR and quantitative real time PCR for cytomegalovirus detection in renal transplant recipients

Significance of nested PCR and quantitative real time PCR for cytomegalovirus detection in renal transplant recipients

Transient versus Persistent BK Viremia and Long-Term Outcomes after Kidney and Kidney–Pancreas Transplantation

Impaired Direct Priming of CD8 T Cells by Donor-Derived Cytomegalovirus Following Kidney Transplantation

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