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Article: Quantification of BK viral load in asymptomatic renal allograft recipients
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TitleQuantification of BK viral load in asymptomatic renal allograft recipients
 
AuthorsChan, GCW1
Leung, AYH1
Wong, ASY1
Chan, KW1
Kwong, YL1
Lai, KN1
Tang, SCW1
 
KeywordsImmunosuppression
Nephropathy
Polyoma BK virus
Quantitative PCR
Renal transplantation
 
Issue Date2012
 
PublisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/0886022x.asp
 
CitationRenal Failure, 2012, v. 34 n. 5, p. 550-554 [How to Cite?]
DOI: http://dx.doi.org/10.3109/0886022X.2012.664808
 
AbstractIntroduction: Polyoma BK virus (BKV) has recently been identified to cause renal allograft dysfunction, which manifests as polyomavirus-associated nephropathy (PVAN). However, the presence and level of BKV DNA in renal allograft patients with good and stable renal function have remained undetermined. Methods: In this prospective study, serum samples were collected from a total of 45 renal allograft recipients with serum creatinine <155 μmol/L. In 17 patients, whose duration of transplantation was under 2 years, samples were collected at 34-month intervals for up to 2 years after transplantation. BK viral load was quantified using quantitative polymerase chain reaction (Q-PCR). Results: The BK viral load in asymptomatic renal allograft recipients was independent of the duration of transplantation and did not correlate with allograft function. The mean (± SD) level of viremia was 552.80 ± 1931.00 genome copies/mL, with 92.9 of patients having low levels of viremia corresponding to <1 × 10 3 copies/mL. In contrast, patients with proven PVAN had levels in the range of 10 6 copies/mL. Conclusions: The prevailing BK viral load in asymptomatic renal allograft patients is quantifiably low. Our findings may guide optimal immunosuppressive modulation in PVAN cases, where judicious manipulation of immunosuppression is required without inciting allograft rejection. Copyright © Informa Healthcare USA, Inc.
 
ISSN0886-022X
2012 Impact Factor: 0.941
2012 SCImago Journal Rankings: 0.383
 
DOIhttp://dx.doi.org/10.3109/0886022X.2012.664808
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorChan, GCW
 
dc.contributor.authorLeung, AYH
 
dc.contributor.authorWong, ASY
 
dc.contributor.authorChan, KW
 
dc.contributor.authorKwong, YL
 
dc.contributor.authorLai, KN
 
dc.contributor.authorTang, SCW
 
dc.date.accessioned2012-09-05T05:32:05Z
 
dc.date.available2012-09-05T05:32:05Z
 
dc.date.issued2012
 
dc.description.abstractIntroduction: Polyoma BK virus (BKV) has recently been identified to cause renal allograft dysfunction, which manifests as polyomavirus-associated nephropathy (PVAN). However, the presence and level of BKV DNA in renal allograft patients with good and stable renal function have remained undetermined. Methods: In this prospective study, serum samples were collected from a total of 45 renal allograft recipients with serum creatinine <155 μmol/L. In 17 patients, whose duration of transplantation was under 2 years, samples were collected at 34-month intervals for up to 2 years after transplantation. BK viral load was quantified using quantitative polymerase chain reaction (Q-PCR). Results: The BK viral load in asymptomatic renal allograft recipients was independent of the duration of transplantation and did not correlate with allograft function. The mean (± SD) level of viremia was 552.80 ± 1931.00 genome copies/mL, with 92.9 of patients having low levels of viremia corresponding to <1 × 10 3 copies/mL. In contrast, patients with proven PVAN had levels in the range of 10 6 copies/mL. Conclusions: The prevailing BK viral load in asymptomatic renal allograft patients is quantifiably low. Our findings may guide optimal immunosuppressive modulation in PVAN cases, where judicious manipulation of immunosuppression is required without inciting allograft rejection. Copyright © Informa Healthcare USA, Inc.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationRenal Failure, 2012, v. 34 n. 5, p. 550-554 [How to Cite?]
DOI: http://dx.doi.org/10.3109/0886022X.2012.664808
 
dc.identifier.doihttp://dx.doi.org/10.3109/0886022X.2012.664808
 
dc.identifier.epage554
 
dc.identifier.hkuros203970
 
dc.identifier.issn0886-022X
2012 Impact Factor: 0.941
2012 SCImago Journal Rankings: 0.383
 
dc.identifier.issue5
 
dc.identifier.pmid22390257
 
dc.identifier.scopuseid_2-s2.0-84860786016
 
dc.identifier.spage550
 
dc.identifier.urihttp://hdl.handle.net/10722/163488
 
dc.identifier.volume34
 
dc.languageeng
 
dc.publisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/0886022x.asp
 
dc.publisher.placeUnited States
 
dc.relation.ispartofRenal Failure
 
dc.relation.referencesReferences in Scopus
 
dc.rightsRenal Failure. Copyright © Informa Healthcare.
 
dc.subject.meshBK Virus - genetics - isolation and purification
 
dc.subject.meshDNA, Viral - analysis
 
dc.subject.meshGraft Rejection - virology
 
dc.subject.meshKidney Diseases - virology
 
dc.subject.meshKidney Transplantation
 
dc.subjectImmunosuppression
 
dc.subjectNephropathy
 
dc.subjectPolyoma BK virus
 
dc.subjectQuantitative PCR
 
dc.subjectRenal transplantation
 
dc.titleQuantification of BK viral load in asymptomatic renal allograft recipients
 
dc.typeArticle
 
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<contributor.author>Leung, AYH</contributor.author>
<contributor.author>Wong, ASY</contributor.author>
<contributor.author>Chan, KW</contributor.author>
<contributor.author>Kwong, YL</contributor.author>
<contributor.author>Lai, KN</contributor.author>
<contributor.author>Tang, SCW</contributor.author>
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<description.abstract>Introduction: Polyoma BK virus (BKV) has recently been identified to cause renal allograft dysfunction, which manifests as polyomavirus-associated nephropathy (PVAN). However, the presence and level of BKV DNA in renal allograft patients with good and stable renal function have remained undetermined. Methods: In this prospective study, serum samples were collected from a total of 45 renal allograft recipients with serum creatinine &lt;155 &#956;mol/L. In 17 patients, whose duration of transplantation was under 2 years, samples were collected at 34-month intervals for up to 2 years after transplantation. BK viral load was quantified using quantitative polymerase chain reaction (Q-PCR). Results: The BK viral load in asymptomatic renal allograft recipients was independent of the duration of transplantation and did not correlate with allograft function. The mean (&#177; SD) level of viremia was 552.80 &#177; 1931.00 genome copies/mL, with 92.9 of patients having low levels of viremia corresponding to &lt;1 &#215; 10 3 copies/mL. In contrast, patients with proven PVAN had levels in the range of 10 6 copies/mL. Conclusions: The prevailing BK viral load in asymptomatic renal allograft patients is quantifiably low. Our findings may guide optimal immunosuppressive modulation in PVAN cases, where judicious manipulation of immunosuppression is required without inciting allograft rejection. Copyright &#169; Informa Healthcare USA, Inc.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong