| Objective: To observe the expression levels of autophagy-related proteins LC3Ⅱ,P62 and p-m TOR in renal tissues of patients with idiopathic membranous nephropathy（IMN）,and to explore their correlations with biochemical indexes,24-hour urine protein quantification and renal interstitial fibrosis,to understand whether the impaired autophagolysosome pathway of renal cells is involved in the occurrence and development of IMN.Methods: From November 2020 to June 2021,42 patients with IMN who were first diagnosed by renal biopsy in our hospital were selected as the experimental group,while 20 patients with renal contusion,ureteral tumor or renal tumor were selected as the control group.1.Analyze and compare the differences of general conditions and clinical indicators between the control group and the experimental group.2.Immunohistochemical method was used to detect the expression of autophagy-related proteins LC3Ⅱ,P62 and p-m TOR in renal tissue cells of IMN group and control group,and the gray value was analyzed.The difference of protein expression between the two groups was compared to understand the performance of autophagolysosome fusion degradation process in IMN.Immunohistochemistry was used to detect the expression of Beclin-1 in renal tissue cells of IMN group and control group,and gray value analysis was performed to understand the performance of autophagy induction process in IMN.3.IMN was divided into fibrosis group（n=23）and non-fibrosis group（n=19）,the differences in the expression of autophagy-related proteins LC3Ⅱ,P62 and p-m TOR between the two groups were analyzed and compared to understand whether autophagy lysosome pathway is involved in the progression of IMN renal interstitial fibrosis.4.Correlation analysis to explore the correlation between the expression of autophagy proteins LC3Ⅱ,P62 and p-m TOR in renal tissue of IMN patients and their general clinical indicators.Results: 1.Compared with the control group,the levels of 24-hour urinary protein,serum triglyceride and total cholesterol in IMN group increased significantly（P<0.01）,while the level of serum albumin decreased significantly（P<0.01）;There was no significant difference in hemoglobin,serum creatinine,blood urea nitrogen,blood uric acid and cystatin C between IMN group and control group（P >0.05）.2.The expressions of LC3Ⅱ,P62 and p-m TOR in renal tissue cells of IMN group were significantly higher than those of normal control group（P <0.01）.The expression of Beclin-1 in renal tissue cells of IMN group was also significantly higher than that of normal control group（P <0.01）.3.The results showed that the expression of LC3Ⅱ and P62 in the fibrosis group of IMN patients was significantly higher than that in the non-fibrosis group（P <0.05）,and there was no significant difference in p-m TOR expression between the fibrosis group and the non-fibrosis group.4.Correlation analysis showed that the expression of LC3Ⅱ,P62 and p-m TOR in renal tissue cells had no correlation with Hb,BUN,Scr,Cys-C（P >0.05）.The expressions of LC3Ⅱ,P62 and p-m TOR were positively correlated with TC,TG and24-hour urinary protein（P <0.01）and negatively correlated with serum albumin level（P< 0.01）.The expression of LC3Ⅱ and P62 was correlated with the level of uric acid in patients（P <0.05）.Conclusion: 1.In IMN patients,the induction of autophagy was enhanced and the number of autophagosomes increased,but the autophagosomes could not function normally to lysosome for degradation,and the autophagy pathway was blocked.The deficiency of autophagy flux caused by the blocked autophagic lysosome degradation of renal cells may be involved in the occurrence and development of IMN.2.The impaired autophagolysosome pathway in renal tissue cells of IMN patients may be involved in the progression of renal interstitial fibrosis.3.The insufficiency of autophagy flux caused by the blocked degradation of autophagy lysosomes in renal tissue cells may be involved in the occurrence and development of IMN. |
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