BK polyomavirus interstitial nephritis in a renal allograft recipient

Kwang Sun Suh; Suk Yeong Kim; Byung Kee Bang; Chul Woo Yang; Jong Min Lee; Joo Hyun Park; Sung Kwon Kim

doi:10.1080/01913120309948

BK polyomavirus interstitial nephritis in a renal allograft recipient

Kwang Sun Suh
, Suk Yeong Kim
, Byung Kee Bang
, Chul Woo Yang
, Jong Min Lee
, Joo Hyun Park
, Sung Kwon Kim

Division of Nephrology

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

Human polyomavirus (PV) interstitial nephritis has recently been recognized as a cause of severe renal allograft dysfunction. It occurs in immunosuppressed patients after reactivation of the latent virus PV type BK (BK virus) in the renal epithelium. BK disease is defined as a morphologically manifest renal infection with cytopathic signs accompanied by varying degrees of interstitial inflammatory cell infiltrates and functional impairment. It is also identified by the presence of cells containing viral inclusion bodies (decoy cells) in the urine. The authors report a case of BK PV interstitial nephritis in a 36-year-old renal allograft recipient. Under light microscopy the chief diagnostic indicator was detection of intranuclear viral inclusions, which were found exclusively in tubular epithelial cells. Cells with viral changes were often enlarged with nuclear atypia and chromatin basophilia. Widespread interstitial plasma cell infiltrates associated with tubulitis were present. Intranuclear paracrystalline arrays of virus particles 35-38 nm in diameter were present as characteristic ultrastructural indicators. Urine samples revealed decoy cells with ground-glass-type intranuclear inclusions positive for BK virus by electron microcopy.

Original language	English
Pages (from-to)	61-64
Number of pages	4
Journal	Ultrastructural Pathology
Volume	27
Issue number	1
DOIs	https://doi.org/10.1080/01913120309948
State	Published - Jan 2003

Bibliographical note

Funding Information:
Received 8 August 2001; accepted 29 August 2001. This work was supported by a 2001 clinical research grant from Chungnam National University Hospital. Address correspondence to Kwang-Sun Suh, MD, Department of Pathology, Chungnam National University School of Medicine, 6, Jung-gu, Munwha-1-dong, Daejeon, Korea, 301^131. E-mail: [email protected]

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

BK polyomavirus
Interstitial nephritis
Renal allograft
Viral inclusions

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10.1080/01913120309948

Cite this

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title = "BK polyomavirus interstitial nephritis in a renal allograft recipient",

abstract = "Human polyomavirus (PV) interstitial nephritis has recently been recognized as a cause of severe renal allograft dysfunction. It occurs in immunosuppressed patients after reactivation of the latent virus PV type BK (BK virus) in the renal epithelium. BK disease is defined as a morphologically manifest renal infection with cytopathic signs accompanied by varying degrees of interstitial inflammatory cell infiltrates and functional impairment. It is also identified by the presence of cells containing viral inclusion bodies (decoy cells) in the urine. The authors report a case of BK PV interstitial nephritis in a 36-year-old renal allograft recipient. Under light microscopy the chief diagnostic indicator was detection of intranuclear viral inclusions, which were found exclusively in tubular epithelial cells. Cells with viral changes were often enlarged with nuclear atypia and chromatin basophilia. Widespread interstitial plasma cell infiltrates associated with tubulitis were present. Intranuclear paracrystalline arrays of virus particles 35-38 nm in diameter were present as characteristic ultrastructural indicators. Urine samples revealed decoy cells with ground-glass-type intranuclear inclusions positive for BK virus by electron microcopy.",

keywords = "BK polyomavirus, Interstitial nephritis, Renal allograft, Viral inclusions",

author = "Suh, \{Kwang Sun\} and Kim, \{Suk Yeong\} and Bang, \{Byung Kee\} and Yang, \{Chul Woo\} and Lee, \{Jong Min\} and Park, \{Joo Hyun\} and Kim, \{Sung Kwon\}",

note = "Funding Information: Received 8 August 2001; accepted 29 August 2001. This work was supported by a 2001 clinical research grant from Chungnam National University Hospital. Address correspondence to Kwang-Sun Suh, MD, Department of Pathology, Chungnam National University School of Medicine, 6, Jung-gu, Munwha-1-dong, Daejeon, Korea, 301\textasciicircum{}131. E-mail: [email protected]",

year = "2003",

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doi = "10.1080/01913120309948",

language = "English",

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T1 - BK polyomavirus interstitial nephritis in a renal allograft recipient

AU - Suh, Kwang Sun

AU - Kim, Suk Yeong

AU - Bang, Byung Kee

AU - Yang, Chul Woo

AU - Lee, Jong Min

AU - Park, Joo Hyun

AU - Kim, Sung Kwon

N1 - Funding Information: Received 8 August 2001; accepted 29 August 2001. This work was supported by a 2001 clinical research grant from Chungnam National University Hospital. Address correspondence to Kwang-Sun Suh, MD, Department of Pathology, Chungnam National University School of Medicine, 6, Jung-gu, Munwha-1-dong, Daejeon, Korea, 301^131. E-mail: [email protected]

PY - 2003/1

Y1 - 2003/1

N2 - Human polyomavirus (PV) interstitial nephritis has recently been recognized as a cause of severe renal allograft dysfunction. It occurs in immunosuppressed patients after reactivation of the latent virus PV type BK (BK virus) in the renal epithelium. BK disease is defined as a morphologically manifest renal infection with cytopathic signs accompanied by varying degrees of interstitial inflammatory cell infiltrates and functional impairment. It is also identified by the presence of cells containing viral inclusion bodies (decoy cells) in the urine. The authors report a case of BK PV interstitial nephritis in a 36-year-old renal allograft recipient. Under light microscopy the chief diagnostic indicator was detection of intranuclear viral inclusions, which were found exclusively in tubular epithelial cells. Cells with viral changes were often enlarged with nuclear atypia and chromatin basophilia. Widespread interstitial plasma cell infiltrates associated with tubulitis were present. Intranuclear paracrystalline arrays of virus particles 35-38 nm in diameter were present as characteristic ultrastructural indicators. Urine samples revealed decoy cells with ground-glass-type intranuclear inclusions positive for BK virus by electron microcopy.

AB - Human polyomavirus (PV) interstitial nephritis has recently been recognized as a cause of severe renal allograft dysfunction. It occurs in immunosuppressed patients after reactivation of the latent virus PV type BK (BK virus) in the renal epithelium. BK disease is defined as a morphologically manifest renal infection with cytopathic signs accompanied by varying degrees of interstitial inflammatory cell infiltrates and functional impairment. It is also identified by the presence of cells containing viral inclusion bodies (decoy cells) in the urine. The authors report a case of BK PV interstitial nephritis in a 36-year-old renal allograft recipient. Under light microscopy the chief diagnostic indicator was detection of intranuclear viral inclusions, which were found exclusively in tubular epithelial cells. Cells with viral changes were often enlarged with nuclear atypia and chromatin basophilia. Widespread interstitial plasma cell infiltrates associated with tubulitis were present. Intranuclear paracrystalline arrays of virus particles 35-38 nm in diameter were present as characteristic ultrastructural indicators. Urine samples revealed decoy cells with ground-glass-type intranuclear inclusions positive for BK virus by electron microcopy.

KW - BK polyomavirus

KW - Interstitial nephritis

KW - Renal allograft

KW - Viral inclusions

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SN - 0191-3123

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BK polyomavirus interstitial nephritis in a renal allograft recipient

Abstract

Bibliographical note

UN SDGs

Keywords

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