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Updated: Apr 20, 2026

Mouse Kidney Transplantation: Models of Allograft Rejection
Published on: October 11, 2014
Effect of transient BK viremia and viruria on long-term renal allograft survival and function
M Koukoulaki1, M Papadaki2, D Pistolas3
1First Department of Surgery, Transplant Unit, Evangelismos General Hospital of Athens, Athens, Greece; Department of Nephrology, Evangelismos General Hospital of Athens, Athens, Greece.
Introduction:
The purpose of this study is to present the five-year survival and function of the renal allograft of recipients who were diagnosed with BK viremia and viruria during the first year after renal transplantation.
Patients And Methods:
BK virus was studied in 32 new renal allograft recipients, from the first postoperative day until 18 months after the transplantation. Real-time polymerase chain reaction was used to detect and quantitate BK viral load in serum and urine samples.
Results:
Qualitative analysis with PCR for the DNA of BK virus showed 31 (31/228, 14%) positive serum samples originating from 20 (20/32, 62%) renal allograft recipients and 57 (57/228, 25%) positive urine samples originating from 23 (23/32, 72%) recipients. During the follow up period of 5 years, renal allograft function remained stable (eGFR 18(th) month: 53.9 ± 23.9 mL/min/1.73 m(2) and eGFR 5(th) year: 52.6 ± 20.6 mL/min/1.73 m(2)). Comparison of recipients that presented with either BK viremia or viruria with a group that did not present viral reactivation did not reveal a statistically significant difference in eGFR. Furthermore, recipients with significantly high viral load in serum or urine did not present renal allograft dysfunction.
Conclusion:
BK virus is potentially pathogenic in renal allograft recipients. It is certain that there is a reactivation of the virus in a high percentage of transplanted patients mostly in the first year after the surgery, without however a negative effect of the transient viremia and viruria in renal allograft function.
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