Background: Few studies on the risk factors for postoperative continuous renal replacement therapy (CRRT) in a homogeneous population of patients with acute type A aortic dissection (AAAD). This retrospective analysis aimed to investigate the risk factors for CRRT and in-hospital mortality in the patients undergoing AAAD surgery and to discuss the perioperative comorbidities and short-term outcomes.Methods: The study collected electronic medical records and laboratory data from 432 patients undergoing surgery for AAAD between March 2009 and June 2021. All the patients were divided into CRRT and non-CRRT groups; those in the CRRT group were divided into the survivor and non-survivor groups. The univariable and multivariable analyses were used to identify the independent risk factors for CRRT and in-hospital mortality.Results: The proportion of requiring CRRT and in-hospital mortality in the patients with CRRT was 14.6 and 46.0%, respectively. Baseline serum creatinine (SCr) [odds ratio (OR), 1.006], cystatin C (OR, 1.438), lung infection (OR, 2.292), second thoracotomy (OR, 5.185), diabetes mellitus (OR, 6.868), AKI stage 2–3 (OR, 22.901) were the independent risk factors for receiving CRRT. In-hospital mortality in the CRRT group (46%) was 4.6 times higher than in the non-CRRT group (10%). In the non-survivor (n = 29) and survivor (n = 34) groups, New York Heart Association (NYHA) class III-IV (OR, 10.272, P = 0.019), lactic acidosis (OR, 10.224, P = 0.019) were the independent risk factors for in-hospital mortality in patients receiving CRRT.Conclusion: There was a high rate of CRRT requirement and high in-hospital mortality after AAAD surgery. The risk factors for CRRT and in-hospital mortality in the patients undergoing AAAD surgery were determined to help identify the high-risk patients and make appropriate clinical decisions. Further randomized controlled studies are urgently needed to establish the risk factors for CRRT and in-hospital mortality.

Background Acute kidney injury (AKI) is a life-threatening complication of rhabdomyolysis (RM). The aim of the present study was to assess patients at high risk for the occurrence of severe AKI defined as stage II or III of KDIGO classification and in-hospital mortality of AKI following RM. Methods We performed a retrospective study of patients with creatine kinase levels > 1000 U/L, who were admitted to the West China Hospital of Sichuan University between January 2011 and March 2019. The sociodemographic, clinical and laboratory data of these patients were obtained from an electronic medical records database, and univariate and multivariate regression analyses were subsequently conducted. Results For the 329 patients included in our study, the incidence of AKI was 61.4% and the proportion of stage I, stage II, stage III were 18.8, 14.9 and 66.3%, respectively. The overall mortality rate was 19.8%; furthermore, patients with AKI tended to have higher mortality rates than those without AKI (24.8% vs. 11.8%; P < 0.01). The clinical conditions most frequently associated with RM were trauma (28.3%), sepsis (14.6%), bee sting (12.8%), thoracic and abdominal surgery (11.2%) and exercise (7.0%). Furthermore, patients with RM resulting from sepsis, bee sting and acute alcoholism were more susceptible to severe AKI. The risk factors for the occurrence of stage II-III AKI among RM patients included hypertension (OR = 2.702), high levels of white blood cell count (OR = 1.054), increased triglycerides (OR = 1.260), low level of high-density lipoprotein cholesterol (OR = 0.318), elevated serum phosphorus (OR = 5.727), 5000<CK ≤ 10,000 U/L (OR = 2.617) and CK>10,000 U/L (OR = 8.093). Age ≥ 60 years (OR = 2.946), sepsis (OR = 3.206) and elevated prothrombin time (OR = 1.079) were independent risk factors for in-hospital mortality in RM patients with AKI. Conclusions AKI is independently associated with mortality in patients with RM, and several risk factors were found to be associated with the occurrence of severe AKI and in-hospital mortality. These findings suggest that, to improve the quality of medical care, the early prevention of AKI should focus on high-risk patients and more effective management.

The aim of the present study was to explore the role of toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88)/nuclear factor (NF)-κB signaling in the contrast-induced injury of renal tubular epithelial cells, and to investigate the potential mechanisms. HK-2 cells cultured in vitro were randomly divided into six groups as follows: i) The blank group; ii) the iohexol group; iii) the NF-κB RNAi group (NF-κB siRNA + iohexol); iv) the TLR4 RNAi group (TLR4 siRNA + iohexol); v) the NF-κB blocker group (PDTC + iohexol); and vi) the TLR4 blocker group (CLI-095 + iohexol). The expression of the TLR4/MyD88/NF-κB signaling pathway proteins was detected by reverse transcription-quantitative (RT-q)PCR and western blot analysis, and the cellular proliferation rate was determined using the Cell Counting Kit-8 assay. The mRNA expression levels of the inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were also detected using RT-qPCR, and apoptosis was assessed by flow cytometry and western blotting to detect apoptosis-associated proteins (caspase-3, caspase-9 and cleaved caspase-9). Compared with the blank group, the apoptotic rates and the expression levels of TLR4, MyD88, NF-κB, caspase-3, cleaved caspase-9, TNF-α, IL-1β and IL-6 were upregulated in the iohexol group (P<0.001). However, when TLR4 or NF-κB were blocked or silenced, these effects were reversed (P<0.001). Collectively, the results of the present study indicated that TLR4/MyD88/NF-κB signaling is involved in the contrast-induced injury of renal tubular epithelial cells by inducing inflammation and apoptosis.

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The aim of the present study was to investigate the effect of erythropoietin (EPO) on contrast-induced nephrology (CIN) in vivo and in vitro. Male C57BL/6J mice were divided into four groups: control, CIN (iohexol 6.0 g/kg), EPO (3,000 IU/kg), and CIN+EPO. Hematoxylin and eosin (H&amp;E) staining and biochemical index analyses were performed to evaluate renal injury. The cellular proliferation rate was detected using the Cell Counting Kit-8 (CCK-8) assay. In addition, a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and flow cytometric assay were used to assess the apoptosis of tissue and cells, respectively. Renal protein expression associated with apoptosis, pyroptosis, and signaling pathways was determined by Western blot (WB) assays for tissues and cells. The results showed that EPO significantly decreased serum creatinine, blood urea nitrogen, and cystatin C levels and alleviated renal histological changes in vivo. The protein levels of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway components were overexpressed in the EPO treatment group. Furthermore, EPO suppressed the cell apoptosis and pyroptosis; decreased the protein levels of cleaved caspase-3, Bax, gasdermin D (GSDMD), and caspase-1; and enhanced the expression of Bcl-2. In summary, EPO could exert renoprotective effect by activating the JAK2/STAT3 signaling pathway, which may be a novel potential therapy for the treatment of CIN in the clinic.