Herpesviruses in patients after renal transplantation

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Abstract

Aim. To estimate graft function after kidney transplantation during active herpesviruses or superinfection

Materials and methods. The study included 32 patients (men – 21, women – 11) with end-stage chronic kidney disease. The median age was 43 years. Cytomegalovirus (CMV), Epstein–Barr virus (EBV) and human herpes virus 6 (HHV-6) DNAs were screened by RT-PCR in the donor's transplant biopsy, and recipients’ peripheral blood and urine after kidney transplantation (KT) on 0, 1, 2, 4, 6, 12 months. Antiviral antibodies (IgM and IgG) were also screened by Enzyme-linked immunoassay analysis (ELISA) along with PCR. The 500 or less copies of viral DNA per 105 nuclear cells or 1 ml of urine was considered as low, more than 1000 copies – high.

Results. On the first month after KT CMV DNA was detected in 50% of pts., EBV DNA – in 40% and HHV-6 DNA – in 33%. During first year after KT two or three viruses simultaneously were found in 12 recipients: CMV, EBV, and HHV-6 were detected in 5 recipients; CMV and EBV – in 4 patients; CMV and HHV-6 – in 2 pts; EBV and HHV-6 – in 1 pt. Graft dysfunction was observed in 9 patients with a high concentration of viral DNA of one, two or three viruses simultaneously. An upraise of the concentration of virus DNA (CMV, EBV and HHV – 6) was detected primarily in the urine, while in the blood its concentration was less than 500 cop or undetectable. Renal dysfunction was not observed on the background of low concentrations of viral DNA in urine and blood. However, with an increase of DNA concentration, an impaired graft function in 8 of 12 patients appeared. Low viral DNA level proved to be a background for another virus activation or bacterial/fungal superinfection.

Conclusion. Graft dysfunction occurs at high viral DNA levels detection during mono-or superinfection. Low viral load can serve as a background for another virus activation and/or bacterial/fungal superinfection.

About the authors

Boldykyz T. Dzhumabaeva

National Research Center for Hematology

Email: bola.blood@yandex.ru
ORCID iD: 0000-0002-7390-2190

д-р мед. наук, вед. науч. сотр. научно-организационного отд. по гематологии, трансфузиологии, донорству

Russian Federation, Moscow

Dmitry S. Tikhomirov

National Research Center for Hematology

Email: bola.blood@yandex.ru
ORCID iD: 0000-0002-2553-6579

канд. мед. наук, ст. науч. сотр. научной лаб. вирусной безопасности трансфузий крови и ее компонентов

Russian Federation, Moscow

Lyudmila S. Biryukova

National Research Center for Hematology

Email: bola.blood@yandex.ru
ORCID iD: 0000-0003-2774-1805

д-р мед. наук, консультат, врач-нефролог отд-ния хирургии

 

Russian Federation, Moscow

Tatiana A. Tupoleva

National Research Center for Hematology

Email: bola.blood@yandex.ru
ORCID iD: 0000-0003-4668-9379

д-р мед. наук, зав. отд. вирусологической диагностики

 

Russian Federation, Moscow

Igor V. Nesterenko

National Research Center for Hematology

Email: bola.blood@yandex.ru
ORCID iD: 0000-0002-1634-3724

д-р мед. наук, врач-хирург отд-ния хирургии

 

Russian Federation, Moscow

Natalia V. Purlo

National Research Center for Hematology

Email: bola.blood@yandex.ru
ORCID iD: 0000-0002-2905-5959

канд. мед. наук, врач-нефролог отд-ния анестезиологии и реанимации

 

Russian Federation, Moscow

Dmitry I. Chebotarev

National Research Center for Hematology

Author for correspondence.
Email: bola.blood@yandex.ru
ORCID iD: 0000-0003-2146-0818

врач-патологоанатом патологоанатомического отд-ния

 

Russian Federation, Moscow

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Supplementary files

Supplementary Files
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1. JATS XML
2. Fig. 1: a – a large necrotic area. On the border with the necrotic tissue, there is a large-caliber artery with an infiltration of its wall by lymphoid cells and a significant narrowing of its lumen due to endothelial proliferation. There is a significant perivascular lymphoid infiltration with single granulocytes, staining with hematoxin-eosin, ×50; b – in the renal parenchyma, lymphoid infiltration is focal and perivascular, there are small foci of tubulitis, staining with hematoxin-eosin, ×200; c – an arteriole with giant cells containing eosinophilic intranuclear inclusions in the arteriole wall (indirect signs of active cytomegalovirus infection), staining with hematoxin-eosin, ×400.

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