BKV viremia.PD-1+, Tim-3+, and CD8+ T cells were evaluated by multiparameter fl ow cytometry.Results: 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.Conclusion: 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.I have no potential conflict of interest to disclose.I did not use generative AI and AI-assisted technologies in the writing process.
Rojas et al. (Wed,) studied this question.