A difficult decision: atypical JC polyomavirus encephalopathy in a kidney transplant recipient

Bialasiewicz, Seweryn, Hart, Gareth, Oliver, Kimberly, Agnihotri, Shruti P., Koralnik, Igor J., Viscidi, Raphael, Nissen, Michael D., Sloots, Theo P., Burke, Michael T., Isbel, Nicole M. and Burke, John (2016) A difficult decision: atypical JC polyomavirus encephalopathy in a kidney transplant recipient. Transplantation, . doi:10.1097/TP.0000000000001275


Author Bialasiewicz, Seweryn
Hart, Gareth
Oliver, Kimberly
Agnihotri, Shruti P.
Koralnik, Igor J.
Viscidi, Raphael
Nissen, Michael D.
Sloots, Theo P.
Burke, Michael T.
Isbel, Nicole M.
Burke, John
Title A difficult decision: atypical JC polyomavirus encephalopathy in a kidney transplant recipient
Journal name Transplantation   Check publisher's open access policy
ISSN 0041-1337
1534-6080
Publication date 2016-06-30
Year available 2016
Sub-type Article (original research)
DOI 10.1097/TP.0000000000001275
Open Access Status Not yet assessed
Total pages 7
Place of publication Philadelphia, PA, United States
Publisher Lippincott Williams & Wilkins
Collection year 2017
Language eng
Formatted abstract
Background: A number of cerebral manifestations are associated with JC polyomavirus (JCPyV) which are diagnosed by detection of JCPyV in cerebrospinal fluid (CSF), often with the support of cerebral imaging. Here we present an unusual case of a kidney transplant patient presenting with progressive neurological deterioration attributed to JCPyV encephalopathy.

Methods: Quantitative polymerase chain reaction JCPyV was used prospectively and retrospectively to track the viral load within the patient blood, urine, CSF, and kidney sections. A JCPyV VP1 enzyme-linked immunosorbent assay was used to measure patient and donor antibody titers. Immunohistochemical staining was used to identify active JCPyV infection within the kidney allograft.

Results: JC polyomavirus was detected in the CSF at the time of presentation. JC polyomavirus was not detected in pretransplant serum, however viral loads increased with time, peaking during the height of the neurological symptoms (1.5E9 copies/mL). No parenchymal brain lesions were evident on imaging, but transient cerebral venous sinus thrombosis was present. Progressive decline in neurological function necessitated immunotherapy cessation and allograft removal, which led to decreasing serum viral loads and resolution of neurological symptoms. JC polyomavirus was detected within the graftʼs collecting duct cells using quantitative polymerase chain reaction and immunohistochemical staining. The patient was JCPyV naive pretransplant, but showed high antibody titers during the neurological symptoms, with the IgM decrease paralleling the viral load after graft removal.

Conclusions: We report a case of atypical JCPyV encephalopathy associated with cerebral venous sinus thrombosis and disseminated primary JCPyV infection originating from the kidney allograft. Clinical improvement followed removal of the allograft and cessation of immunosuppression.
Keyword JC polyomavirus (JCPyV)
Cerebrospinal fluid (CSF)
Kidney transplant
Kidney allograft
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

 
Versions
Version Filter Type
Citation counts: Scopus Citation Count Cited 0 times in Scopus Article
Google Scholar Search Google Scholar
Created: Tue, 26 Jul 2016, 01:08:40 EST by System User on behalf of Learning and Research Services (UQ Library)