Clinical and immunological characteristics for BK polyomavirus-associated nephropathy after kidney transplantation.

INTRODUCTION: BK polyomavirus (BKPyV)-associated nephropathy (BKPyVAN) can cause a significant risk of allograft impairment after kidney transplantation (KT). Intact BKPyV-specific immunity is associated with viral containment. This study investigated BKPyV-specific immunological factors among KT recipients. METHODS: This prospective study in a single transplant center from January 2019 to August 2019 assessed associations between clinical and immunological characteristics, with a focus on BKPyV-cell-specific immunity and BKPyVAN, among KT recipients aged ≥15 years. The numbers of interferon-gamma (IFN-γ)-producing CD4+  T, CD8+  T, natural killer (NK), and natural killer T (NKT) cells were measured after stimulation with large T antigen and viral capsid protein 1 (VP1). RESULTS: In total, 100 KT recipients were included (mean age ± SD, 42 ± 11 years); 35% of the recipients were female patients, and 70% had received induction immunosuppressive therapy. The 1-year cumulative incidence of high-level BKPyV DNAuria (possible BKPyVAN) and (presumptive BKPyVAN) was 18%. Among 40 patients with immunological factor data, pre-KT %NK cells (hazard ratio [HR], 1.258; 95% confidence interval [CI], 1.077-1.469; p = .004) and %VP1-specific NK cells (HR, 1.209; 95% CI, 1.055-1.386; p = .006) were factors independently associated with possible and presumptive BKPyVAN. KT recipients with possible and presumptive BKPyVAN were more likely to exhibit significant mean coefficients of %NK, %VP1-specific NK, and %NKT cells at 1 month after KT than before KT (all p < .05). CONCLUSION: Individuals with nonspecific and VP1-specific NK cells before KT and increasing numbers of these cells after KT may be at risk for high-level BKPyV DNAuria and presumptive BKPyVAN. Further studies are needed to determine the utility of BKPyV-specific innate immune surveillance in predicting the occurrence of BKPyVAN.

Improving inpatient glycemic control by diabetes education program in internal medicine residents.

AIMS: The purpose of this study was to investigate the effectiveness of an inpatient diabetes care education during the first year of internal medicine residency training on inpatient glycemic control. METHODS: The program was comprised of 1-hr small group teaching per 4-week rotation and twice-a-week morning insulin round by an endocrinologist. Inpatient insulin management guideline leaflet was provided to all internal medicine residents. We retrospectively collected the point-of-care testing for glucose (POCT-glu) data in patients admitted to the general medicine wards and compared the mean of blood glucose (BG) before and after the education program. A total of 134438 POCT-glu values from 7055 patients were analyzed. RESULTS: After the initiation of the education program, mean BG levels significantly decreased during the first year and were lowest during the second year after education (Mean BG at baseline was 161.38 ±â€¯64.10 mg/dL; 1st year, 159.48 ±â€¯62.53 mg/dL and 2nd year, 155.60 ±â€¯64.94 mg/dL, p-value < 0.0001). The reduction of BG levels was more pronounced in the patients with previously undiagnosed diabetes mellitus than patients with underlying diabetes mellitus. The rates of severe hypoglycemia (defined by BG < 40 mg/dL or 2.2 mmol/L) were not significantly different before and after education (baseline 0.12%, 1st year 0.14%, and 2nd year 0.14%, p-value = 0.632). CONCLUSIONS: Lack of confidence and inadequate knowledge of insulin treatment in physicians were important barriers to glycemic management. Consistent education in internal medicine residents led to a significant improvement in inpatient glycemic control.