Early initiation of RRT for patients with AKI is not associated with decreased overall mortality or a delayed renal recovery rate. The optimal time to initiate RRT remains uncertain. Large scale and adequately powered RCTs are needed to detect the effects of early initiation of RRT in AKI patients.
Isoflurane, a widely used volatile anesthetic, induces neuronal apoptosis and memory impairments in various animal models. However, the potential mechanisms and effective pharmacologic agents are still not fully understood. The p38MAPK/ATF-2 pathway has been proved to regulate neuronal cell survival and inflammation. Besides, atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, exerts neuroprotective effects. Thus, this study aimed to explore the influence of atorvastatin on isoflurane-induced neurodegeneration and underlying mechanisms. Aged C57BL/6 mice (20 months old) were exposed to isoflurane (1.5%) anesthesia for 6 h. Atorvastatin (5, 10, or 20 mg/kg body weight) was administered to the mice for 7 days. Atorvastatin attenuated the isoflurane-induced generation of ROS and apoptosis. Western blotting revealed a decrease in cleaved caspase-9 and caspase-3 expression in line with ROS levels. Furthermore, atorvastatin ameliorated the isoflurane-induced activation of p38MAPK/ATF-2 signaling. In a cellular study, we proved that isoflurane could induce oxidative stress and inflammation by activating the p38MAPK/ATF-2 pathway in BV-2 microglia cells. In addition, SB203580, a selected p38MAPK inhibitor, inhibited the isoflurane-induced inflammation, oxidative stress, and apoptosis. The results implied that p38MAPK/ATF-2 was a potential target for the treatment of postoperative cognitive dysfunction.
Vitamin C plus saline administration is effective at reducing the risk of CI-AKI. Evidence for the use of vitamin E plus saline in this context is encouraging, but more trials are required. Furthermore, this meta-analysis and TSA indicated insufficient power to draw a definitive conclusion on the effect of vitamin C plus NAC, versus saline or NAC alone, which needs to be explored further.
Background: Considering transaminase more than the upper limit of normal value as liver injury might overestimate the prevalence of liver involvement in COVID-19 patients. No meta-analysis has explored the impact of varied definitions of liver injury on the reported prevalence of liver injury. Moreover, few studies reported the extent of hypertransaminasemia stratified by COVID-19 disease severity. Methods: A literature search was conducted using PubMed and Embase. The pooled prevalence of liver injury and hypertransaminasemia was estimated. Results: In total, 60 studies were included. The overall prevalence of liver injury was 25%. Compared to subgroups with the non-strict definition of liver injury (33%) and subgroups without giving detailed definition (26%), the subgroup with a strict definition had a much lower prevalence of liver injury (9%). The overall prevalence of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) elevation was 19% and 22%. The prevalence of elevated ALT and AST were significantly higher in severe COVID-19 cases compare to non-severe cases (31% vs 16% and 44% vs 11%). In critically ill and fatal cases, no difference was found in the prevalence of elevated ALT (24% vs 30%) or AST (54% vs 49%). Sensitivity analyses indicated that the adjusted prevalence of ALT elevation, AST elevation, and liver injury decreased to 14%, 7%, and 12%.
Conclusion:The overall prevalence of liver injury and hypertransaminasemia in COVID-19 patients might be overestimated. Only a small fraction of COVID-19 patients have clinically significant liver injury. The prevalence of hypertransaminasemia was significantly higher in severe COVID-19 cases compare to non-severe cases. Hence, in severe COVID-19 patients, more attention should be paid to liver function tests.
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