| Objective and Background:IgAN (IgA nephropathy, IgAN) is one of the most common primary glomerulonephritis in the global, but its pathogenesis is still unclear.The abnormal glycosylation of IgA molecule deposition in the mesangial area causes kidney injure.The oxidation and antioxidant imbalance of IgAN patients can aggravates the progression of the disease.The innate immune disorders also will caused surface antigen on mucosal can not be cleard, IgA molecule synthesis changes and inflammation reaction.They can aggravates the progression of IgAN.The above is some research progress about IgAN pathogenesis.A lot of literature prove that the complement system activation plays an important role in the occurrence of IgAN.The purpose of this study is to investigate the C3a deposition in IgAN renal tissue, and C3aR expression in IgA nephropathy.We hope some new pathogenesis can be found in the of IgAN, thereby to provide a new method of thinking in clinical. This experiment is to investigate the role and expression of C3a and its receptor in the IgAN pathogenesis.Subjects and Methods:Selecting83cases of Lee’s Ⅱ, Ⅲ, level Ⅳ IgAN patients with renal biopsy specimens as the case group from the deparment of nephrology of the first affiliated hospital of Zhengzhou University form January to December in2011.And selecting10cases of kidney tumor resection in patients with normal renal tissue as a control.We apply immunohistochemical methods to detect C3a, C3aR expression in renal tissue of IgAN.Selecting18cases of Lee’s Ⅱ, Ⅲ, Ⅳ grade IgAN renal biopsy specimens as the experimental group from the deparment of nephrology of the first affiliated hospital of Zhengzhou University form August to December in2011,and four cases of renal biopsy specimens of patients with minimal change(MCD) as the control group,we detect the C3aRmRNA expression in renal tissue by RT-PCR technique.Result:C3a deposits at the renal tissue of different levels of IgAN,increasing with the aggravation of pathological damage. C3aR are expressed in different levels of IgA nephropathy tissue, its expression also increases with the aggravation of pathological damage.Compared with the control group,the expression of C3amRNA in IgAN tissue increases significantly.As the pathology grade increasing, the expression of C3aRmRNA is also increasing in IgAN tissue.Conclusion:There are lots of C3a deposition in IgAN tissue,closely associatting with IgA nephropathy tissue damage.There are also lots of C3aR expressing on the IgAN tissue,causing the renal tissue damage by ligand binding. C3a and its receptor may play an important role in the pathogenesis of IgAN. We can improve IgAN renal tissue injury extent by inhibitting C3a and usingthe C3aR antagonist. |
