Clin Transplant Res 2024; 38(2): 71-89
Published online June 30, 2024
https://doi.org/10.4285/ctr.24.0006
© The Korean Society for Transplantation
Department of Pathology, Cedars-Sinai Medical Center, Los Angeles, CA, USA
Correspondence to: Cynthia C. Nast
Department of Pathology, Cedars-Sinai Medical Center, Room 8612, 8700 Beverly Blvd, Los Angeles, CA 90048, USA
E-mail: Cynthia.Nast@cshs.org
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Polyomaviruses, particularly BK virus, are ubiquitous latent infections that may reactivate with immunosuppression during kidney transplantation, resulting in polyomavirus nephropathy (PVN). The levels of viruria and viremia serve as tools for screening and making a presumptive diagnosis of PVN, respectively, while a definitive diagnosis requires a kidney biopsy. There are histologic classifications of PVN based on the extent of tubular cell viral infection, interstitial fibrosis, and interstitial inflammation. These classifications correlate to some degree with graft function and loss, aiding in determining treatment efficacy and prognostication. PVN has histologic overlap with acute cell-mediated rejection, making the differential diagnosis challenging, although there are suggestive features for these different causes of graft dysfunction. This article reviews the diagnosis, histologic findings, and classifications of PVN, and discusses how to differentiate viral nephropathy from acute rejection.
Keywords: Polyomavirus, BK virus, Viremia, Kidney biopsy, Graft rejection
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