Introduction: Some patients with COVID-19 pneumonia present systemic disease involving multiple systems. There is limited information about the clinical characteristics and events leading to acute kidney injury (AKI). We described the factors associated with the development of AKI and explored the relation of AKI and mortality in Mexican population with severe COVID-19. Methods: We retrospectively reviewed the medical records of individuals with severe pneumonia caused by SARS-CoV-2 hospitalized at the largest third-level reference institution for COVID-19 care in Mexico between March and April 2020. Demographic information, comorbidities, clinical and laboratory data, dates of invasive mechanical ventilation (IMV) and hospitalization, mechanical-ventilator settings and use of vasoactive drugs were recorded. Results: Of 99 patients studied, 58 developed AKI (58.6%). The risk factors for AKI were older age (OR = 1.07, 95% CI = 1.01–1.13, p = 0.024); obesity (OR = 6.58, 95% CI = 1.8–24.05, p = 0.040); and the need for IMV (OR = 6.18, CI = 1.29–29.58, p = 0.023). The risk factors for mortality were obesity (OR = 5.57, 95% CI = 1.48–20.93, p = 0.011); requirement of vasoactive drugs on admission (OR = 5.35, 95% CI = 1.16–24.61, p = 0.031); and AKI (OR = 8.61, 95% CI = 2.24–33.1, p = 0.002). In-hospital mortality was significantly higher in patients with AKI stage 3 (79.3%) and AKI stage 2 (68.7%) compared with those with AKI stage 1 (25%; p = 0.004). Fifty-three patients underwent the furosemide stress test (FST) to predict progression to AKI stage 3. Of those, 12 progressed to AKI stage 3 (22%). The ROC curve for the FST had an AUC of 0.681 (p = 0.009); a sensitivity of 81.6% and a specificity of 54.5%. Conclusions: AKI was common in our cohort of patients with severe pneumonia caused by SARS-CoV-2 infection. The risk factors for AKI were older age, obesity and the need for of IMV on admission. The risk factors for mortality were obesity, requirement of vasoactive drugs on admission and AKI. Mortality was more frequent in patients with AKI stages 2–3. The FST had an acceptable predictive capacity to identify patients progressing to AKI stage 3.

A high proportion of critically ill patients with COVID-19 develop acute kidney injury (AKI) and die. The early recognition of subclinical AKI could contribute to AKI prevention. Therefore, this study was aimed at exploring the role of the urinary biomarkers NGAL and [TIMP-2] × [IGFBP7] for the early detection of AKI in this population. This prospective, longitudinal cohort study included critically ill COVID-19 patients without AKI at study entry. Urine samples were collected on admission to critical care areas for determination of NGAL and [TIMP-2] × [IGFBP7] concentrations. The demographic information, comorbidities, clinical, and laboratory data were recorded. The study outcomes were the development of AKI and mortality during hospitalization. Of the 51 individuals that were studied, 25 developed AKI during hospitalization (49%). Of those, 12 had persistent AKI (23.5%). The risk factors for AKI were male gender (HR = 7.57, 95% CI: 1.28–44.8; p = 0.026) and [TIMP-2] × [IGFBP7] ≥ 0.2 (ng/mL)²/1000 (HR = 7.23, 95% CI: 0.99–52.4; p = 0.050). Mortality during hospitalization was significantly higher in the group with AKI than in the group without AKI (p = 0.004). Persistent AKI was a risk factor for mortality (HR = 7.42, 95% CI: 1.04–53.04; p = 0.046). AKI was frequent in critically ill COVID-19 patients. The combination of [TIMP-2] × [IGFBP7] together with clinical information, were useful for the identification of subclinical AKI in critically ill COVID-19 patients. The role of additional biomarkers and their possible combinations for detection of AKI in ritically ill COVID-19 patients remains to be explored in large clinical trials.

Objective: Around 20–30% of HIV-infected individuals (HIV+) on successful antiretroviral therapy (ART) fail to normalize their CD4⁺ T-cell counts. Various factors could contribute to the lack of immune reconstitution, one of them being thymic insufficiency. We aimed to explore associations between recent thymic emigrants (RTEs) and CD4⁺ T-cell recovery. Design: ART-naive HIV+ individuals who started ART with advanced AIDS were selected. Good versus poor immune reconstitution was defined by CD4⁺ gains above or below 100 CD4⁺ T cells/μl. The follow-up period was 6 months. Methods: Peripheral blood mononuclear cells were isolated and flow cytometry was used to characterize RTEs as the fraction of naive CD4⁺ T cells expressing CD31⁺, the platelet endothelial cell adhesion molecule. Markers of cellular activation, senescence, exhaustion and cycling were also assessed. Results: After 6 months on ART, HIV+ individuals with good immune reconstitution had higher absolute numbers of RTEs, compared with those with poor immune reconstitution, and these strongly correlated with CD4⁺ gains in those individuals with good immune reconstitution but not with poor immune reconstitution. We also found that CD8⁺ T-cell immune activation decreased as early as 2 months post-ART initiation in individuals with good immune reconstitution, but only at month 6 post-ART in individuals with poor immune reconstitution. Levels of immune activation were inversely correlated with the absolute numbers of RTEs in both groups, but more strongly so in individuals with poor immune reconstitution. Conclusion: We show that RTEs are linked to CD4⁺ T-cell recovery and that the degree of immune reconstitution is not directly linked to persistent immune activation.

In order to discriminate general from aetiology-specific risk factors for immune reconstitution inflammatory syndrome (IRIS), we followed up, during six months, 99 patients with advanced HIV infection commencing antiretroviral therapy (ART) without active opportunistic infections or evident inflammation. IRIS predictors were determined by univariate analysis using clinical data from 76 ART-responding patients either completing follow-up or developing IRIS, and by multivariate analysis of inflammation, disease progression and nutrition status variables. We identified 23 primary IRIS events (30.3%). Univariate predictors for all IRIS events were higher platelet counts and lower CD4/CD8 ratio, whereas subclinical inflammation was the multivariate predictor. Platelets, alkaline phosphatase levels and %CD8 T-cells in univariate analysis also predicted mycobacteria-associated IRIS independently, remaining elevated during follow-up. Herpesvirus IRIS was predicted by platelets and inflammation. Indicators of advanced HIV disease and subclinical inflammation jointly predict IRIS, and some are specific of the underlying microbial aetiology, possibly explaining previous reports.

Background: Damage due to respiratory viruses increases the risk of bacterial and fungal coinfections and superinfections. High rates of invasive aspergillosis are seen in severe influenza and COVID‐19. This report describes CAPA cases diagnosed during the first wave in the biggest reference centre for severe COVID‐19 in Mexico.Objectives: To describe the clinical, microbiological and radiological characteristics of patients with invasive pulmonary aspergillosis associated with critical COVID‐19, as well as to describe the variables associated with mortality.Methods: This retrospective study identified CAPA cases among individuals with COVID‐19 and ARDS, hospitalised from 1 March 2020 to 31 March 2021. CAPA was defined according to ECMM/ISHAM consensus criteria. Prevalence was estimated. Clinical and microbiological characteristics including bacterial superinfections, antifungal susceptibility testing and outcomes were documented.Results: Possible CAPA was diagnosed in 86 patients among 2080 individuals with severe COVID‐19, representing 4.13% prevalence. All CAPA cases had a positive respiratory culture for Aspergillus species. Aspergillus fumigatus was the most frequent isolate (64%, n = 55/86). Seven isolates (9%, n = 7/80) were resistant to amphotericin B (A. fumigatus n = 5/55, 9%; A. niger, n = 2/7, 28%), two A. fumigatus isolates were resistant to itraconazole (3.6%, n = 2/55). Tracheal galactomannan values ranged between 1.2 and 4.05, while serum galactomannan was positive only in 11% (n = 3/26). Bacterial coinfection were documented in 46% (n = 40/86). Gram negatives were the most frequent cause (77%, n = 31/40 isolates), from which 13% (n = 4/31) were reported as multidrug‐resistant bacteria. Mortality rate was 60% and worse prognosis was seen in older persons, high tracheal galactomannan index and high HbA1c level.Conclusions: One in 10 individuals with CAPA carry a resistant Aspergillus isolate and/or will be affected by a MDR bacteria. High mortality rates are seen in this population.