Background: Polyomavirus BK virus infection is a significant complication of renal transplantation and is an important cause of allograft loss. Today, despite the innovations in the pharmaceutical industry, a curative treatment against the BK virus has not been developed. The management is not standardized and is generally based on reported experience from transplantation centers. However, the literature on the subject with large samples is limited. Therefore, we designed a study to present our countrywide experience with BK virus nephropathy (BKVN) in renal transplant recipients. Methods: Our study was conducted with thirty kidney transplant centers from all provinces of Turkey. Only cases with BKVN proven by allograft biopsy were included in our study. Demographic characteristics and laboratory values of the patients were obtained from the archives and electronic databases of the centers. Results: A total of 13.857 patients from 30 transplantation centers were screened. 207 BKVN cases proven by allograft biopsy were identified and included in the study. The mean age was 46.4±13.1, and 146 (70.5%) patients were male. Twenty-six patients did not receive any induction therapy, 144 patients received anti-T lymphocyte globulin (ATLG), and 37 patients received basiliximab after transplantation. 23.6% of the patients had acute rejection history in the first six months of renal transplantation. all were treated with pulse steroids, and 46 were also treated with ATLG. The mean time to diagnosis of BKVN was 15.8±22.2 months after transplantation. At the time of diagnosis, the patients’ mean creatinine level was 1.8±0.7 mg/dl, and the mean estimated glomerular filtration rate was 45.8±19.6 ml/min. While BKVN was solely reported in 181 cases, there were cellular rejection findings in 21 biopsy specimens and humoral rejection in 4 biopsy specimens. In addition of dose reduction or discontinuation of immunosuppressive drugs, eighteen patients were treated with cidofovir, 11 patients with leflunomide, 17 patients with quinolones, 15 patients with intravenous immunoglobulin (IVIG), five patients with cidofovir+IVIG, and 12 patients with leflunomide+IVIG. None of the patients who received leflunomide and leflunomide+IVIG had allograft loss. Allograft loss was observed in 12 (15%) of 78 patients treated with antivirals or immunomodulators. Allograft loss occurred in 32 patients (15%) during follow-up out of 207 patients with BKVN. Five patients were retransplanted, and none developed BKVN during the follow-up. Conclusions: BKVN is still a significant cause of allograft loss in kidney transplantation, which has not been fully elucidated. Leflunomide appears to be an effective treatment in these patients.

Background: Although changes of the main lymphocyte subsets (T cells, T helper, T cytotoxic, B cells, NK cells) and lymhocyte activation status in COVID-19 patients have been reported, the results of the studies differ each other. Therefore, we aimed to determine lymphocyte subgroups and activation status of them with flow cytometry at the time of diagnosis in COVID-19 patients and examine the relation of them with disease stage and length of hospital stay. Methods: Fourty patients included in the study were compared with the age and sex matched 40 healthy controls. COVID-19 patients were divided into 2 groups as mild and severe stage disease. Flow cytometry assay was performed to examine the numbers of lymphocyte subsets and activation status of them. Total lymphocyte count was calculated and CD45, CD3, CD4, CD8, CD19, CD27, CD38, CD56, CD57, IgD were studied on lymphocyte gate. T helper / T cytotoxic rates and length of hospital stay were recorded. Results: The patients’ CD3(+)CD4(+) ( T helper) count and CD27 expression on T cells counts were significantly lower, and CD57 expression on CD3(+)CD8(+) T cytotoxic cells were significantly higher (p<0.05) than control gruop. When the patients were divided into mild and severe stages, it was observed that CD38 expression on T cells were significantly lower in severe stage patients (p< 0.05) Total lymphocyte count and CD3(+) T lymphocyte count were negatively correlated with the lengt of hospital stay as statistically significant (p <0.05). Conclusion: Our data showed that the SARS-CoV-2 primarly effects on T lymphocytes. It was thought that this effect occured by impairment of development and activation of T lymphocytes. There are some discordances among the studies on T lympocytes in the literature. Studies with more patients are needed to make this information more reliable.