ABSTRACT
OBJECTIVE@#To assess the predictors and outcomes of acute kidney injury (AKI) among patients with coronavirus disease 2019 (COVID-19).@*OBJECTIVE@#This retrospective observational study was conducted among patients with a confirmed diagnosis of COVID-19 admitted to Hankou Hospital between January, 5 and March 8, 2020. We evaluated the association of AKI with the demographic and biochemical parameters and clinical outcomes of the patients using univariate regression analysis.@*OBJECTIVE@#Atotal of 287 COVID-19 patients, including 55 with AKI and 232 without AKI, were included in the analysis. Compared with the patients without AKI, the patients with AKI were older, predominantly male, and were more likely to have hypoxia and pre-existing hypertension and cerebrovascular diseases. The patients with AKI also had higher levels of white blood cells, D-dimer, aspartate aminotransferase, total bilirubin, creatine kinase, lactate dehydrogenase, procalcitonin, C-reactive protein, a higher prevalence of hyperkalemia, lower lymphocyte counts, and higher chest computed tomographic scores. The incidence of stage 1 AKI was 14.3% and that of stage 2 or 3 AKI was 4.9%. The patients with AKI had much higher mortality rate than those without AKI.@*OBJECTIVE@#AKI is an important complication of COVID-19. An older age, a male gender, multiple pre- existing comorbidities, lymphopenia, increased infection indicators, elevated D-dimer, and impaired heart and liver functions are all potential risk factors ofAKI. COVID- 19 patients with AKI that progresses into stages 2 or 3 AKI have a high mortality rate. Prevention of AKI and monitoring kidney function is critical in the care of COVID-19 patients.
Subject(s)
Aged , Humans , Male , Acute Kidney Injury/epidemiology , COVID-19 , China/epidemiology , Retrospective Studies , SARS-CoV-2ABSTRACT
Genipin (GP) is commonly used to treat cardiovascular diseases; however, the protective action of GP against vascular hyperpermeability (VH) has not been reported. We previously reported that intrinsic apoptotic signaling (IAS) is involved in VH following hemorrhagic shock (HS). GP inhibits apoptosis, but the specific mechanism remains unclear. In the present study, we observed that GP protects against HS-induced VH in vitro and in vivo. We report that this protective effect is related to the inhibition of IAS by up-regulation of autophagy via sirtuin 3 (SIRT3). The endothelial cell hyperpermeability induced by HS was enhanced by GP; this was attenuated by 3-methyladenine (3MA), a specific inhibitor of autophagy, indicating the involvement of autophagy. Consistent with these results, we found that 3MA reversed the effects of GP on up-regulation of autophagy, and also diminished the protective effect of GP against IAS activation following HS. Furthermore, knockout of SIRT3 inhibited GP-induced autophagy, indicating the requirement of SIRT3 in the regulation of autophagy by GP. In rats, GP improved HS-induced VH, which was repressed by 3MA and 3-(1H-1,2,3-triazol-4-yl)pyridine (3-TYP), a SIRT3 inhibitor. In conclusion, these findings suggest that autophagy plays a protective effect in VH following HS; the protective effect of autophagy is reinforced by GP, which protects against IAS and VH by up-regulating SIRT3.
ABSTRACT
Objective To investigate the effects of drag-reducing polymers on microcirculation in 40%total body surface area burn-injured rats. Methods SD rats were randomized into control group, drag-reducing polymer (DRPs) group and normal saline (NS) group (5 minutes after scald, drag-reducing polymer or saline was injected for fluid resuscitation). Wet dry weigh ratio of lung, histopathologic changes and arterial blood gas at 24 hour were respectively measured by wet dry weigh ratio method, hematoxylin-eosin (HE) staining and arterial blood gas analysis. The velocity of flow of red cell in oblique ridge and the survival time of burn-injured rats were observed. Results Compared with control group, rats in NS group exhibit significant lung injury characterized by a high W/D (P < 0.01), accumulation of a large number of neutrophils in HE stain, low partial pressure of oxygen (PO2) and high lactate (Lac) (P<0.05 or P<0.01) in arterial blood. Compared with the NS group, DRPs treatment rats exhibit significantly reduced lung injury characterized by W/D reducing (P < 0.05), the reduction of neutrophil infiltration, increased PO2, decreased Lac (P<0.05, P<0.01). In addition, DRPs treatment obviously increases the burn-induced low velocity of flow of red cell in oblique ridge (P<0.01). Moreover, the survival time of burned rats can be improved by DRPs treatment (P < 0.05). Conclusion DRPs ameliorates burn-induced acute lung injury, the mechanism may be through improving the burn-induced microcirculation disorders.
