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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
BK virus (BKV) is a signifi cant cause of chronic kidney injury in kidney transplant recipients that results in allograft loss. The common clinical manifestations range from asymptomatic viral viremia to BKV-associated nephropathy (BKVN). However, there is no standardized approach to monitoring and management of BKV after pediatric kidney transplantation. Inhibitory receptors programmed death 1 (PD-1) and T-cell Ig and mucin domain-containing molecule-3 (Tim-3) play a crucial role in regulating CD8+ T cell function during chronic infection. The study’s aim 1 was to determine the clinical characteristics of those who had BK viremia versus those who did not. Aim 2 was to document correlation between exhausted PD-1+ and Tim-3+ exhausted T cells during chronic BKV infection.
The retrospective case-control study was conducted from January 2008 to July 2022 in the Children’s Hospital, China Medical University. The subjects were composed of a total of 32 pediatric kidney transplant recipients (KTRs) and 12 with BKV viremia, in which 5 of 12 had BKV-associated nephropathy were obtained. Peripheral blood mononuclear cells (PBMCs) were collected during episodes of BKV viremia. PD-1+, Tim-3+, and CD8+ T cells were evaluated by multiparameter fl ow cytometry.
BKV viremia was observed in 12/32 (37.5%) and BKVN in 5/32 (15.6%). Induction therapy was not significantly different between BKV and non-BKV viremia groups. The mean time for BK detection was 4.1 months after renal transplantation. Percent rise in serum creatinine correlated with intensity of viral load. There were no signifi cant differences in sex, age, type of transplantation donor and type of renal diagnosis (glomerulonephritis, non-glomerulonephritis or monogenic gene defect), induction and maintenance therapy. The first-line therapy after identification of BKV viremia was a decreased dosage in Tacrolimus (100%) and intravenous immunoglobulin, and discontinuing mycophenolate mofetil. When reduction in immunosuppressant was not suffi cient to decrease viral load, 4/12 (33.3%) of patients received lefl unomide. High expression of PD-1+ and Tim-3+ on CD8+ T cells with more severe T cells exhaustion was noted during chronic BKV infection. The treatment resistance was also accompanied with persistent high level of PD-1+ and Tim-3+ expression on CD8+ T cells. There was no difference in the percentage of graft survival between BKV viremia and non-BKV viremia after 8 years’ follow-up.
Patients with the highest viral loads and longest duration of BKV viremia are at risk of BKVN. Expression of PD-1+, Tim-3+ and CD8+ T cell indicates chronic T cell partial exhaustion. BKV viremia and CD8+ T cell exhaustion may be a surrogate marker for adjusting immunosuppressant reduction and intravenous immunoglobulin treatment.
