Abstract
BackgroundSepsis 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.Methods207 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)-1β 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.ResultsThe Scr levels in the patients were significantly decreased after treatment with CRRT. Before treatment, the IL-1β 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-1β, IL-6, LC3-II and Beclin-1, but not Atg-5 values were significantly correlated with Scr.ConclusionThe 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.
Highlights
Sepsis is one of the common death factors in intensive care unit, which refers to the systemic inflammatory response syndrome caused by infection
Expression of autophagy-related genes of the patients before and after treatment The expressions of autophagy-related proteins, i.e., light chain 3 (LC3)-II, autophagy-related 5 (Atg-5) and Beclin-1, in the monocytes of the patients peripheral blood were detected by means of Quantitative reverse transcription polymerase chain reaction (qRT-PCR)
Expressions of autophagy-related genes of the survived and died patients after one to three weeks after the treatment LC3-phosphatidylethanolamine conjugate (LC3-II), Atg-5 and Beclin-1 expressions measured through qRT-PCR in the monocytes showed that the expressions of autophagy-related proteins (LC3-II, Atg-5 and Beclin-1) were significantly (p < 0.001) elevated in
Summary
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. Beclin-1 is a key protein that regulates autophagy and cell death, and studies have revealed that Beclin-1 is differentially expressed in the renal tissues of rat models of renal ischemia-reperfusion injury [4,5,6,7,8]
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