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BK virus nephropathy in renal transplant recipients

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NEPHROLOGY
卷 21, 期 8, 页码 647-654

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WILEY-BLACKWELL
DOI: 10.1111/nep.12728

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polyoma BK virus; transplant dysfunction; two-hit hypothesis

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BK virus nephropathy (BKVN) occurs in up to 10% of renal transplant recipients and can result in graft loss. The reactivation of BK virus in renal transplant recipients is largely asymptomatic, and routine surveillance especially in the first 12-24 months after transplant is necessary for early recognition and intervention. Reduced immunosuppression and anti-viral treatment in the early stages may be effective in stopping BK virus replication. Urinary decoy cells, although highly specific, lack sensitivity to diagnose BKVN. Transplant biopsy remains the gold standard to diagnose BKVN, good surrogate markers for surveillance using quantitative urinary decoy cells, urinary SV40 T immunochemical staining or polyoma virus-Haufen bodies are offered by recent studies. Advanced BKVN results in severe tubulo-interstitial damage and graft failure. Retransplantation after BKVN is associated with good outcomes. Newer treatment modalities are emerging.

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