Introduction Data on antibody response following COVID-19 in kidney transplant recipients is scarce. We performed a cross-sectional study to investigate antibody response to COVID-19 among kidney transplant recipients. Design We recruited 46 kidney transplant recipients with RT-PCR confirmed COVID-19 and 45 recipients without COVID-19 history. We also constructed two control groups (COVID-19 positive and negative) from a historical cohort of health care workers. We used age and sex-based propensity score matching to select eligible subjects to control groups. We measured SARS-Cov-2 IgG levels quantitatively using the Abbott ARCHITECT system. An antibody level above 1.4 S/C defined positivity. Results Transplant recipients with COVID-19 had a higher BMI, and COVID-19 history in a household member was more common than that of the transplant recipient without COVID-19. IgG seropositivity rate (69.6% vs 78.3%, p=0.238) and median IgG level (3.28 [IQR 0.80-5.85] vs 4.59 [1.61-6.06], p=0.499) were similar in COVID-19 positive transplant recipients and controls. There was a trend toward lower antibody levels in kidney transplant recipients associated with a longer duration between RT-PCR and antibody testing (r=-0.532, p<0.001). Conclusion At the early post-COVID-19 period, transplant recipients have an antibody response that is similar to controls. However, antibody levels and associated immunity should be closely observed with longer follow-up durations.

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 Real-life data on the predialysis management of chronic kidney disease (CKD) is scarce. We aimed to investigate the current clinical practice and compliance among nephrologists with KDIGO CKD mineral bone disorders (MBD) guidelines. Methods We performed a multicenter cross-sectional study. We recruited stage 3-5 non-dialysis (ND) CKD patients and recorded data related to CKD MBD from two consecutive outpatient clinical visits apart 3 to 6 months. We calculated therapeutic inertia for hyperphosphatemia, hypocalcemia, hyperparathyroidism, and hypovitaminosis D and overtreatment for hypophosphatemia, hypercalcemia, hypoparathyroidism, and hypervitaminosis D. Results We examined a total of 302 patients (male: 48.7%, median age: 67 years). The persistence of low 25-OH vitamin D levels (61.7%) was the most common laboratory abnormality related to CKD-MBD, followed by hyperparathyroidism (14.8%), hyperphosphatemia (7.9%), and hypocalcemia (0.0%). According to our results, therapeutic inertia seems to be a more common problem than overtreatment for all the CKD-MBD laboratory parameters that we examined. Therapeutic inertia frequency was highest for hypovitaminosis D (81.1%), followed by hypocalcemia (75.0%), hyperparathyroidism (59.0%), and hyperphosphatemia (30.4%), respectively. Conclusion We found that CKD-MBD is not optimally managed in CKD stage 3-5 ND patients. Clinicians should have an active attitude regarding the correction of MBD even at the earlier stages of CKD.