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Transpl Int. 2015 Sep;28(9):1081-91. doi: 10.1111/tri.12601. Epub 2015 May 22.

Different risk factor profiles distinguish early-onset from late-onset BKV-replication.

Author information

1
Department of Nephrology and Internal Intensive Care, Charité University Medicine Berlin, Berlin, Germany.
2
Berlin-Brandenburg Center of Regenerative Therapies (BCRT), Berlin, Germany.

Abstract

Two of three reactivations of latent BKV-infection occur within the first 6 months after renal transplantation. However, a clear differentiation between early-onset and late-onset BKV-replication is lacking. Here, we studied all kidney transplant recipients (KTRs) at our single transplant center between 2004 and 2012. A total of 103 of 862 KTRs were diagnosed with BK viremia (11.9%), among which 24 KTRs (2.8%) showed progression to BKV-associated nephropathy (BKVN). Sixty-seven KTRs with early-onset BKV-replication (65%) and 36 KTRs with late-onset BKV-replication (35%) were identified. A control group of 598 KTRs without BKV-replication was used for comparison. Lymphocyte-depleting induction, CMV-reactivation, and acute rejection increased the risk of early-onset BKV-replication (P < 0.05). Presensitized KTRs undergoing renal retransplantation were those at increased risk of late-onset BKV-replication (P < 0.05). Among KTRs with BK viremia, higher doses of mycophenolate increased the risk of progression to BKVN (P = 0.004). KTRs with progression to BKVN showed inferior allograft function (P < 0.05). KTRs with late-onset BK viremia were more likely not to recover to baseline creatinine after BKV-replication (P = 0.018). Our data suggest different risk factors in the pathogenesis of early-onset and late-onset BKV-reactivation. While a more intensified immunosuppression is associated with early-onset BKV-replication, a chronic inflammatory state in presensitized KTRs may contribute to late-onset BKV-replication.

KEYWORDS:

BK polyomavirus; CMV; renal transplantation

PMID:
25959355
DOI:
10.1111/tri.12601
[Indexed for MEDLINE]
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