Background we aimed to explore the relationship of acute kidney injury (AKI) with the severity and mortality of coronavirus disease 2019 (COVID-19). Methods A systematic literature search was conducted in PubMed, EMBASE, Scopus, Web of Science, MedRxiv Database. We compared the laboratory indicators of renal impairment and incidences of AKI in the severe versus non-severe cases, and survival versus non-survival cases, respectively. Results In 41 studies with 10,335 COVID-19 patients, the serum creatinine (sCr) in severe cases was much higher than that in non-severe cases (SMD = 0.34, 95% CI: 0.29–0.39), with a similar trend for blood urea nitrogen (BUN) (SMD = 0.66, 95%CI: 0.51–0.81), hematuria (OR = 1.59, 95% CI: 1.15–2.19), and proteinuria (OR = 2.92, 95% CI: 1.58–5.38). The estimated glomerular filtration rate decreased significantly in severe cases compared with non-severe cases (SMD = -0.45, 95% CI: −0.67–0.23). Moreover, the pooled OR of continuous renal replacement therapy (CRRT) and AKI prevalence for severe vs. non-severe cases was 12.99 (95%CI: 4.03–41.89) and 13.16 (95%CI: 10.16–17.05), respectively. Additionally, 11 studies with 3759 COVID-19 patients were included for analysis of disease mortality. The results showed the levels of sCr and BUN in non-survival cases remarkably elevated compared with survival patients, respectively (SMD = 0.97, SMD = 1.49). The pooled OR of CRRT and AKI prevalence for non-survival vs. survival cases was 31.51 (95%CI: 6.55–151.59) and 77.48 (95%CI: 24.52–244.85), respectively. Conclusions AKI is closely related with severity and mortality of COVID-19, which gives awareness for doctors to pay more attention for risk screening, early identification and timely treatment of AKI.

Immune dysregulation characterized by T cell exhaustion and high level of inflammatory cytokines is associated with severe COVID-19. Figuring out the early event of immune dysregulation would provide a potential treatment for COVID-19. Recent evidence indicate that mitochondrial dysfunction participates in the development of COVID-19 and may be responsible for the dysregulated immune response. Mitochondrial-targeted ubiquinone (MitoQ), a mitochondrial-targeted antioxidant, shows beneficial effects on various diseases through improving mitochondrial dysfunction. We hypothesize that MitoQ could act as a potential treatment in COVID-19. MitoQ may alleviate cytokine storm and restore the function of exhausted T cells in COVID-19 patients through improving mitochondrial dysfunction. In this article, we provide evidence to support the use of MitoQ as a potential treatment or adjunct therapy in the context of COVID-19.

Background The impact of pre-existing interstitial lung disease (ILD) on the severity and mortality of COVID-19 remains largely unknown. The purpose of this meta-analysis was to investigate the prevalence of ILD among patients with COVID-19 and figure out the relationship between ILD and the poor clinical outcomes of COVID-19. Methods A systematic literature search was conducted in the PubMed, EMBASE, Web of Science and MedRxiv Database from 1 January 2020 to 26 May 2021. Results 15 studies with 135,263 COVID-19 patients were included for analysis of ILD prevalence. The pooled prevalence of comorbid ILD in patients with COVID-19 was 1.4% (95% CI, 1.1%-1.8%, I 2 = 91%) with significant between-study heterogeneity. Moreover, the prevalence of ILD in non-survival patients with COVID-19 was 2.728-folds higher than that in corresponding survival patients (RR = 2.728, 95% CI 1.162–6.408, I 2 = 54%, p = 0.021). Additionally, 2–3 studies were included for comparison analysis of clinical outcome between COVID-19 patients with and without ILD. The results showed that the mortality of COVID-19 patients with ILD was remarkably elevated compared with patients without ILD (RR = 2.454, 95% CI 1.111–5.421, I 2 = 87%, p = 0.026). Meanwhile, the pooled RR of ICU admission for ILD vs. non-ILD cases with COVID-19 was 3.064 (95% CI 1.889–4.972, I 2 = 0, p < 0.0001). No significant difference in utilizing rate of mechanical ventilation was observed between COVID-19 patients with and without ILD. Conclusions There is great variability in ILD prevalence among patients with COVID-19 across the globe. Pre-existing ILD is associated with higher severity and mortality of COVID-19.

Introduction We aimed to describe the respiratory supports and determine their association with clinical outcomes of COVID-19 patients in intensive care unit (ICU). Methods A systemic literature search was conducted in PubMed, EMBASE, MedRxiv and BioRxiv database from December 2019 to 2 July 2020. Studies reporting the application of respiratory supports in COVID-19 patients admitted to ICU were included. Results Forty studies with 15320 COVID-19 patients were included in this systematic review. The proportion of invasive mechanical ventilation (IMV) application in ICU patients with COVID-19 was 73.8%. Further analysis elucidated that the use rate of IMV in Asia, Europe and North America was 47%, 76.2% and 80.2%, respectively. The proportion of patients treated with prone positioning and IMV was 29.4%. 25.5% of COVID-19 patients requiring IMV developed ventilator-associated pneumonia. The mortality of patients treated with IMV was 51.1%, while only 17.5% of critically ill COVID-19 patients treated with non-IMV respiratory support died. Additionally, the utilization rate of IMV in non-survival patients was shown 17.26-folds (95%CI 2.89–103.24, p = 0.002) higher than that in survival patients, while the use rate of ECMO was no significant difference. Conclusions Our findings highlight respiratory supports of COVID-19 patients admitted to ICU in different continents. IMV is a life-saving strategy for critically ill COVID-19 patients with ARDS, yet the mortality remains very high.

In this study, we aimed to investigate the effect of electro-acupuncture (EA) at the Zusanli acupoint (ST36) on interleukin (IL)-33-mediated mast cell activation. Firstly, 2,4-dinitrofluorobenzene (DNFB)-induced allergic contact dermatitis (ACD) in rats was developed with or without EA treatment. Then, rat peritoneal mast cells (RPMCs) were obtained and cultured in the presence of IL-33. EA treatment relieved ear swelling and reduced mast cell infiltration in the local inflammation area with DNFB challenge, accompanying the decrement of IL-33 production. RPMCs isolated from ACD rats with EA treatment showed significant downregulation of IL-6, TNF-α, IL-13, and MCP-1 production following IL-33 stimulation. However, there was no obvious difference in surface ST2 receptor expression among different groups. In addition, EA selectively altered IL-33 signaling, suppressing p38 phosphorylation as well as NF-κB- and AP-1-mediated transcription but not Akt phosphorylation. Importantly, EA lowered microRNA (miR)-155 expression in the RPMCs, which presented a positive correlation with IL-33-induced IL-6 production. Furthermore, overexpression of miR-155 in the RPMCs was established following miR-155 mimic transfection. RPMCs with the overexpressed miR-155 displayed an obvious increment of inflammatory cytokine and abrogated the inhibitive effect of EA on NF-κB- and AP-1-regulated transcription in response to IL-33 compared with those without transfected-miR-155. These findings demonstrate EA treatment inhibits NF-κB and AP-1 activation as well as promotes the negative feedback regulation of IL-33 signaling via targeting miR-155 in mast cells, which contribute to the anti-inflammatory effect of EA on DNFB-induced ACD in rats.