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Background Vitamin D status has been implicated in COVID-19 disease. The objective of the COVID-VIT-D trial was to investigate if an oral bolus of cholecalciferol (100,000 IU) administered at hospital admission influences the outcomes of moderate-severe COVID-19 disease. In the same cohort, the association between baseline serum calcidiol levels with the same outcomes was also analysed. Methods The COVID-VIT-D is a multicentre, international, randomised, open label, clinical trial conducted throughout 1 year. Patients older than 18 years with moderate-severe COVID-19 disease requiring hospitalisation were included. At admission, patients were randomised 1:1 to receive a single oral bolus of cholecalciferol ( n =274) or nothing ( n =269). Patients were followed from admission to discharge or death. Length of hospitalisation, admission to intensive care unit (ICU) and mortality were assessed. Results In the randomised trial, comorbidities, biomarkers, symptoms and drugs used did not differ between groups. Median serum calcidiol in the cholecalciferol and control groups were 17.0 vs . 16.1 ng/mL at admission and 29.0 vs . 16.4 ng/mL at discharge, respectively. The median length of hospitalisation (10.0 [95%CI 9.0–10.5] vs . 9.5 [95%CI 9.0–10.5] days), admission to ICU (17.2% [95%CI 13.0–22.3] vs. 16.4% [95%CI 12.3–21.4]) and death rate (8.0% [95%CI 5.2–12.1] vs . 5.6% [95%CI 3.3–9.2]) did not differ between the cholecalciferol and control group. In the cohort analyses, the highest serum calcidiol category at admission (>25ng/mL) was associated with lower percentage of pulmonary involvement and better outcomes. Conclusions The randomised clinical trial showed the administration of an oral bolus of 100,000 IU of cholecalciferol at hospital admission did not improve the outcomes of the COVID-19 disease. A cohort analysis showed that serum calcidiol at hospital admission was associated with outcomes. Trial registration COVID-VIT-D trial was authorised by the Spanish Agency for Medicines and Health products (AEMPS) and registered in European Union Drug Regulating Authorities Clinical Trials (EudraCT 2020-002274-28) and in ClinicalTrials.gov ( NCT04552951 ).

Background and Objectives: We developed a predictive statistical model to identify donor–recipient characteristics related to kidney graft survival in the Chilean population. Given the large number of potential predictors relative to the sample size, we implemented an automated variable selection mechanism that could be revised in future studies as more national data is collected. Materials and Methods: A retrospective multicenter study was conducted to analyze data from 822 adult kidney transplant recipients from adult donors between 1998 and 2018. To the best of our knowledge, this is the largest kidney transplant database to date in Chile. A procedure based on a cross-validated regularized Cox regression using the Elastic Net penalty was applied to objectively identify predictors of death-censored graft failure. Hazard ratios were estimated by adjusting a multivariate Cox regression with the selected predictors. Results: Seven variables were associated with the risk of death-censored graft failure; four from the donor: age (HR = 1.02, 95% CI: 1.00–1.03), male sex (HR = 0.64, 95% CI: 0.46–0.90), history of hypertension (HR = 1.49, 95% CI: 0.98–2.28), and history of diabetes (HR = 2.04, 95% CI: 0.97–4.29); two from the recipient: years on dialysis log-transformation (HR = 1.29, 95% CI: 0.99–1.67) and history of previous solid organ transplantation (HR = 2.02, 95% CI: 1.18–3.47); and one from the transplant: number of HLA mismatches (HR = 1.13, 95% CI: 0.99–1.28). Only the latter is considered for patient prioritization in deceased kidney allocation in Chile. Conclusions: A risk model for kidney graft failure was developed and trained for the Chilean population, providing objective criteria which can be used to improve efficiency in deceased kidney allocation.

MicroRNAs control the differentiation and function of B cells, which are considered key elements in the pathogenesis of systemic lupus erythematosus (SLE). However, a common micro(mi)RNA signature has not emerged since published data includes patients of variable ethnic background, type of disease, and organ involvement, as well as heterogeneous cell populations. Here, we aimed at identifying a miRNA signature of purified B cells from renal and non-renal severe SLE patients of Latin American background, a population known to express severe disease. Genome-wide miRNA expression analyses were performed on naive and memory B cells and revealed two categories of miRNA signatures. The first signature represents B cell subset-specific miRNAs deregulated in SLE: 11 and six miRNAs discriminating naive and memory B cells of SLE patients from healthy controls (HC), respectively. Whether the miRNA was up or down-regulated in memory B cells as compared with naive B cells in HC, this difference was abolished in SLE patients, and vice versa. The second signature identifies six miRNAs associated with specific pathologic features affecting renal outcome, providing a further understanding for SLE pathogenesis. Overall, the present work provided promising biomarkers in molecular diagnostics for disease severity as well as potential new targets for therapeutic intervention in SLE.