RESUMEN
This study investigated whether autophagy is activated after sepsis-induced acute kidney injury (AKI) and explored its biological role. Seventy-two normal C57 mice were randomly divided into sham operation group, cecal ligation and puncture (CLP) group and CLP+3-MA (autophagy inhibitor) group; 24 mice in each group. Mice in CLP and CLP+3-MA group were treated with cecal ligation to establish sepsis, while mice in sham operation group were treated with the same surgical operations, but not cecal ligation. Blood samples were collected from 12 mice of each group and the levels of serum creatinine (Cr) and blood urea nitrogen (BUN) were measured. The pathological changes were observed. The remaining 12 mice in each group were kept and the survival rate was recorded. Changes in the expressions of autophagy-related proteins were detected by reverse transcription-semi-quantitative PCR and western blotting. The results revealed that the levels of Cr and BUN in CLP and CLP+3-MA group were significantly higher than those in sham operation group (P<0.05), and the levels of Cr and BUN in CLP+3-MA group were higher than those in CLP group (P<0.05). The pathological score of renal injury in CLP+3-MA group was significantly higher than that of CLP group (P<0.01). The expression levels of Beclin1 and LC3-II/I were significantly increased in CLP group compared to sham operation group (P<0.01), while the expression of p62 was decreased (P<0.01). After 3-MA treatment the expression levels of Beclin1 and LC3-II/I were decreased, compared with CLP group, but accumulation of p62 occurred, and the degree of renal injury was increased. In conclusion, AKI induced by sepsis in mice can induce apoptosis and activate autophagy. The activation of autophagy aggravates the renal injury in mice, which in turn inhibits AKI after sepsis.
RESUMEN
BACKGROUND: Sepsis is one of the common death factors in intensive care unit, which refers to the systemic inflammatory response syndrome caused by infection. It has many complications such as acute renal injury, shock, multiple organ dysfunction, and failure. The mortality of acute renal injury is the highest among the complications, which is a serious threat to the safety of patients and affects the quality of life. This study aimed to observe the changes in autophagy-related protein expressions in patients with acute kidney injury (AKI) after continuous renal replacement therapy (CRRT) and their impacts on prognosis. METHODS: 207 AKI patients visiting the Emergency Department of The First People's Hospital of Xuzhou from January 2014 to February 2018 were recruited and treated with CRRT. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was applied to detect the expression of autophagy-related genes, including light chain 3 type II (LC3-II), autophagy-related 5 (Atg-5) and Beclin-1, in the monocytes of the patient's peripheral blood before and after treatment. The levels of inflammatory mediators interleukin (IL)-1ß and IL-6 were determined via enzyme-linked immunosorbent assay before and after treatment. The patient's serum creatinine (Scr) level before and after treatment was measured using a full-automatic biochemistry analyser. Moreover, the treatment effect was graded after CRRT, and the relationship between the prognosis of patients and the autophagy-related proteins was observed. RESULTS: The Scr levels in the patients were significantly decreased after treatment with CRRT. Before treatment, the IL-1ß and IL-6 blood levels were high in the patients, while the amounts were significantly reduced after CRTT. The expressions of LC3-II, Atg-5 and Beclin-1 in the monocytes of patients after treatment were significantly decreased compared with those before treatment. Compared with those in survived patients, the expression of autophagy-related proteins was significantly elevated in in patients died after one to three weeks after the treatment. IL-1ß, IL-6, LC3-II and Beclin-1, but not Atg-5 values were significantly correlated with Scr. CONCLUSION: The expression of LC3-II, Atg-5 and Beclin-1 in the monocytes of patients may change prominently after treatment with CRRT, so they are expected to be regarded as new prognostic indicators for AKI patients.
RESUMEN
The aim of the present study was to examine the effects of continuous renal replacement therapy (CRRT) on pyemic secondary acute kidney injury (AKI) by serum cartilage glycoprotein 39 (YKL-40) and Annexin A1. From October, 2013 to October, 2015, 45 pyemic secondary AKI cases and 40 pyemic non-secondary AKI cases were selected for the present study. There were also 35 cases of physical examination volunteers. The serum YKL-40 and Annexin A1 levels were compared. CRRT was applied to pyemic secondary AKI patients and based on the obtained results the patients were divided into the success and failure groups. YKL-40, Annexin A1, hs-CRP, creatinine and urea nitrogen levels after 1, 6, 12, 24, 48 and 72 h of AKI were measured. The YKL-40 and Annexin A1 levels in the pyemic secondary AKI group were significantly higher than those in other two groups and differences were statistically significant (P<0.05). There was no statistically significant difference regarding time period for applying CRRT in the success and failure groups (P>0.05). The peak level of YKL-40 and Annexin A1 in the success group decreased more rapidly compared to the failure group and the difference was statistically significant (P<0.05). When the differences in creatinine and urea nitrogen levels at different time points were compared between the success and failure groups, no statistical significance was observed (P>0.05). However, the success group showed a significantly lower level compared to the failure group at 72 h. Comparisons for other time periods showed no statistical significance (P>0.05). Thus, the serum cartilage glycoprotein 39 and Annexin A1 level were able to predict the clinical effects of CRRT on pyemic secondary AKI.
RESUMEN
BACKGROUND: To investigate the clinical value of real-time three-dimensional echocardiography (RT-3DE) for assessing of left ventricular systolic synchronicity. METHODS: Thirty healthy volunteers and 62 patients with congestive heart failure (CHF) were enrolled. The SD of time to peak systolic motion (TDI-Ts12-SD) was measured with tissue Doppler imaging in 12 myocardial segments. The SD and maximal difference of the time to minimal systolic volume (Tmsv) between 16, 12, or 6 myocardial segments, expressed as a percentage of cardiac cycle duration, were measured with RT-3DE and labeled Tmsv16-SD%, Tmsv12-SD%, Tmsv6-SD%, Tmsv16-D%, Tmsv12-D%, and Tmsv6-D%, respectively. The Spearman coefficient and Kappa value were calculated, and Bland-Altman analysis was performed to investigate the correlation and agreement between the two methods. Tmsv values were compared with ejection fraction (EF). RESULTS: There was a moderately positive (p< 0.01) correlation between TDI-Ts12-SD and Tmsv16-SD%, Tmsv12-SD%, Tmsv16-D%, and Tmsv12-D% (r = 0.65, 0.64, and 0.65, respectively, with Kappa values of 0.66, 0.65, 0.72, and 0.74, respectively, p< 0.01). Tmsv16-SD%, Tmsv12-SD%, and Tmsv12-D% were significantly different between CHF patients with EF ≤ 35% and those with EF > 35%. CONCLUSIONS: RT-3DE can be used in patients with CHF to quantify left ventricular mechanical dyssynchrony. Tmsv12-SD% and Tmsv12-D% were the best indices of left ventricular systolic synchronicity in relation to the severity of CHF as evaluated from EF.