BK nephropathy in pediatric hematopoietic stem cell transplant recipients

Authors

  • Priya S. Verghese,

    1. Department of Pediatrics, University of Washington and Seattle Children’s Hospital, Seattle, WA, USA
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  • Laura S. Finn,

    1. Department of Laboratory and Pathology, University of Washington and Seattle Children’s Hospital, Seattle, WA, USA
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  • Janet A. Englund,

    1. Department of Pediatrics, University of Washington and Seattle Children’s Hospital, Seattle, WA, USA
    2. Fred Hutchinson Cancer Research Center and Seattle Children’s Hospital, Seattle, WA, USA
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  • Jean E. Sanders,

    1. Department of Pediatrics, University of Washington and Seattle Children’s Hospital, Seattle, WA, USA
    2. Fred Hutchinson Cancer Research Center and Seattle Children’s Hospital, Seattle, WA, USA
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  • Sangeeta R. Hingorani

    1. Department of Pediatrics, University of Washington and Seattle Children’s Hospital, Seattle, WA, USA
    2. Fred Hutchinson Cancer Research Center and Seattle Children’s Hospital, Seattle, WA, USA
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Priya S. Verghese, MD, Division of Nephrology, Children’s Hospital and Regional Medical Center, 4800 Sand Point Way, NE, Seattle, WA 98105, USA
Tel: +206 987 2524
Fax: +206 987 2636
E-mail: priya.verghese@seattlechildrens.org

Abstract

Abstract:  BK nephropathy is a known cause of renal insufficiency in kidney transplant recipients. Activation of the polyoma virus may also occur in the native kidneys of non-renal allograft recipients. BK nephropathy has only been reported in a few patients after HCT, most being adult patients, and the single reported pediatric case had evidence of hemorrhagic cystitis. The response to antiviral therapy also seems to differ widely. Here, we describe two cases of BK nephropathy in the native kidneys of HCT recipients exposed to high levels of immunosuppression because of GVHD. Neither of our patients had any evidence of hemorrhagic cystitis. We present definitive renal pathology and detailed chronological evidence of the rising serum creatinine with simultaneous serum and urine BK PCR titers. In one of our cases, antiviral therapy did not seem beneficial as documented by continued renal dysfunction and elevated serum/urine BK PCR titers. Based on our report, intense immunosuppression in pediatric HCT recipients seems to be involved in the activation of BK virus and BK nephropathy should be suspected even in the absence of hematuria in HCT recipients with unexplained renal dysfunction.

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