Introduction: The high transmissibility and lethality of the novel coronavirus SARS-CoV-2 (COVID-19) have been catastrophic. Acute kidney injury (AKI) is one of the frequent complications in patients with respiratory insufficiency caused by the virus. The pathogenic mechanism is based on the binding of its S-proteins to the angiotensin-converting enzyme (ACE) receptors, which will trigger a cellular damage. A podocyte and tubular compromise are found in the kidneys which can lead to tubular necrosis and the consequent AKI. Objectives: The objective of this report is to identify the main risk factor to develop AKI in patients infected with SARS-CoV-2 with critical acute respiratory distress. Patients and Methods: We performed this report study, collecting data from 48 ICU patients. Data from 13 of them who developed AKI and needed renal replacement therapy (RRT)were analyzed. Clinical characteristics and laboratory findings were reported using STATA 10.0. Results: AKI was present in 27.08% of patients, mostly male (92.3%) with a mean age of 63.8 years old. Hypertension, diabetes and obesity were the main comorbidities in those patients. Additionally, the meantime between admission and AKI diagnosis was 2.69 days. All patients showed fibrinogen, D-dimer, ALT and values above normal range. Mortality was seen in 61.5% of patients. Conclusion: This report tries to show AKI as an important clinical manifestation in critically ill patients infected with SARS-CoV-2, with high mortality. Further studies are needed to demonstrate if there are independent risk factors. / Revisión por pares

Introduction: Only 3 types of coronavirus cause aggressive respiratory disease in humans (MERS-Cov, SARS-Cov-1, and SARS-Cov-2). It has been reported higher infection rates and severe manifestations (ICU admission, need for mechanical ventilation, and death) in patients with comorbidities such as diabetes mellitus (DM). For this reason, this study aimed to determine the prevalence of diabetes comorbidity and its associated unfavorable health outcomes in patients with acute respiratory syndromes for coronavirus disease according to virus types. Methods: Systematic review of literature in Pubmed/Medline, Scopus, Web of Science, Cochrane, and Scielo until April of 2020. We included cohort and cross-sectional studies with no restriction by language or geographical zone. The selection and extraction were undertaken by 2 reviewers, independently. The study quality was evaluated with Loney’s instrument and data were synthesized by random effects model meta-analysis. The heterogeneity was quantified using an I2 statistic. Funnel plot, Egger, and Begg tests were used to evaluate publication biases, and subgroups and sensitivity analyses were performed. Finally, we used the GRADE approach to assess the evidence certainty (PROSPERO: CRD42020178049). Results: We conducted the pooled analysis of 28 studies (n = 5960). The prevalence analysis according to virus type were 451.9 diabetes cases per 1000 infected patients (95% CI: 356.74-548.78; I2 = 89.71%) in MERS-Cov; 90.38 per 1000 (95% CI: 67.17-118.38) in SARS-Cov-1; and 100.42 per 1000 (95% CI: 77.85, 125.26 I2 = 67.94%) in SARS-Cov-2. The mortality rate were 36%, 6%, 10% and for MERS-Cov, SARS-Cov-1, and SARS-Cov-2, respectively. Due to the high risk of bias (75% of studies had very low quality), high heterogeneity (I2 higher than 60%), and publication bias (for MERS-Cov studies), we down rate the certainty to very low. Conclusion: The prevalence of DM in patients with acute respiratory syndrome due to coronaviruses is high, predominantly with MERS-Cov infection. The unfavorable health outcomes are frequent in this subset of patients. Well-powered and population-based studies are needed, including detailed DM clinical profile (such as glycemic control, DM complications, and treatment regimens), comorbidities, and SARS-Cov-2 evolution to reevaluate the worldwide prevalence of this comorbidity and to typify clinical phenotypes with differential risk within the subpopulation of DM patients. / Revisión por pares

40% of severe acute respiratory syndrome coronavirus two (SARS-CoV-2) severe cases develop acute kidney injury (AKI). Current treatment for renal complications limits financial and material resources available. To explore alternative treatments and accelerate research in case of future coronavirus outbreaks, a mouse model of coronavirus disease 2019-associated AKI (C19-AKI) would represent a critical biomedical research tool. The surrogate model of C19-AKI (SMC) developed consisted of angiotensin-converting enzyme two (ACE2) knockout (KO) mice receiving 400 ng/kg/min of angiotensin (Ang) II by osmotic minipump for eight days with a single injection of lipopolysaccharide (LPS; 10 mg/kg) on the seventh day of Ang II and euthanasia 24 hours after LPS. Similarly, to C19-AKI, the SMC exhibited albuminuria, elevated blood urea nitrogen, electrolyte imbalance, neutrophil infiltration, and upregulation of the G-coupled protein receptor (GPR)84 and pro-inflammatory and injury markers. GPR84 was found in bronchoalveolar lavage fluid neutrophils of coronavirus disease 2019 (COVID-19) patients, suggesting a potential implication of GPR84 in the disease. We hypothesised that GPR84 deletion or antagonism with GLPG-1205 could attenuate SMC’s indices of renal injury and inflammation. GLPG-1205 and GPR84 KO had no effects in the SMC model, as suggested by unchanged albuminuria, electrolytes, and markers expression. Interestingly, neutrophil infiltration was attenuated by GLPG-1205 only. The SMC is an interesting tool for therapeutic development for infections associated with renal injury, such as SARS-CoV-2. GPR84 role in the SMC needs to be further assessed.