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Comparative Study
. 2014 Mar;9(3):553-61.
doi: 10.2215/CJN.08420813. Epub 2014 Jan 9.

Transient versus persistent BK viremia and long-term outcomes after kidney and kidney-pancreas transplantation

Affiliations
Comparative Study

Transient versus persistent BK viremia and long-term outcomes after kidney and kidney-pancreas transplantation

Nissreen Elfadawy et al. Clin J Am Soc Nephrol. 2014 Mar.

Abstract

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 (1.75±0.6) and transient high viremia (1.85±0.7) groups compared with aviremic controls (1.47±0.4; 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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Figures

Figure 1.
Figure 1.
Patient survival by Kaplan‐Meier analysis in the selected study population. (A) Overall, patient survival was 95.2% at a median follow-up of 36 (range=3–66) months, which was not significantly different for the five groups stratified by BK viremia persistence and viral loads (log-rank P=0.10). (B) Graft survival by Kaplan–Meier analysis in the selected study population. Overall, patient survival was 92.6% at a median follow-up of 36 (range=3–66) months, which was not significantly different for the five groups stratified by BK viremia persistence and viral loads (log rank P=0.60).
Figure 2.
Figure 2.
Graft rejection by Kaplan–Meier analysis. There is a significant difference in the long-term graft rejection rates among the five groups (21.5% rejection in negative polyomavirus BK [BKV] infection, 17.3% rejection in persistent low viremia, 19% rejection in transient low viremia, 34% rejection in persistent high viremia, and 50% rejection in transient high viremia; log-rank P=0.01).

References

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