| Background:The pathogenesis of IgAN(IgA nephropathy)is still unclear.Correlational studies have found that more than 50%of IgAN patients with end-stage renal disease can relapse within 2 years after renal transplantation,and IgA molecules were found deposited in donor's kidneys again by renal pathological biopsy.However,IgA deposition in non-IgAN uremic patients can disappear within a few weeks after renal transplant as the donor were IgAN patients.Therefore,the pathogenesis of IgAN should not be limited to the kidney itself.Recent studies have shown that macrophages are involved in renal fibrosis,leading to the development of chronic kidney disease.It is considered that the distribution of macrophages in the kidney could be used as an important indicator to judge the progression and prognosis of kidney diseases.However,macrophages can be divided into M0,M1 and M2 types.Which type of macrophages play a leading role in IgAN renal fibrosis and cause disease progression?There is no final conclusion.In addition,the deposition of galactose deficient IgA1(Gd-IgA1)and its immune complexes in the kidney is the core mechanism of IgAN,which can trigger a series of immune responses by activating complement,involving a variety of immune cells and related cytokines.Macrophages are involved in renal interstitial fibrosis(RIF),leading to the progression of IgAN.Therefore,we speculate that certain types of macrophages are mainly involved in the pathological progress of IgAN(including renal fibrosis),and serum Gd-IgAl may directly cause renal fibrosis by regulating macrophages.Objective:To detect the distribution of different types of renal macrophages and the concentration of serum Gd-IgA1 of IgAN patients,and to explore the relationship between Gd-IgA1/macrophages and clinical indexes,renal fibrosis(TGF ?1)and pathological grade(Oxford classification).Methods:Peripheral blood samples and paraffin specimens of renal tissue of 40 IgAN patients confirmed by clinical and renal pathology in Subei Hospital of Jiangsu Province were selected as the observation group.At the same time,peripheral blood of 14 healthy volunteers,and paraffin specimens of normal renal tissue and peripheral blood of 6 patients treated by nephrectomy in our hospital due to trauma were used as the normal control group.M0,M1 and M2 macrophages were labeled with CD68,CD80 and CD 163 respectively.The distribution of macrophages and the expression of TGF?1 were detected by immunofluorescence and/or immunohistochemistry.The concentration of serum Gd-IgAl was detected by km55 ELISA kit to analyse the relationship between Gd-IgA1 and macrophages in renal fibrosis.Results:1.The number of M0,M1,M2macrophages could be found increased in IgAN patients.MO macrophages are mainly polarized towards M2.The number of M2 macrophages was positively correlated with creatinine and urinary protein levels,and negatively correlated with eGFR.The number of M2 macrophages was positively correlated with Oxford classification T,which increased with the rise of pathological grade T.The number of MO and Ml macrophages were not found involved in clinical parameters and Oxford classification.2.The number of M2 macrophages was significantly positively correlated with the degree of renal fibrosis and TGF ?1.The number of M0 and M1 macrophages were not found correlated with the degree of renal fibrosis and TGF ?1.3.The concentration of serum Gd-IgAl increased significantly in IgAN patients,but it was not correlated with clinical parameters and Oxford classification.4.There was no significant correlation between the concentration of serum Gd-IgAl and the distribution of renal TGF ?1/M2 macrophages in IgAN patients.Conclusion:The number of different types of renal macrophages in IgAN patients increased significantly,among which M2 macrophages are involved in the progression of disease and renal fibrosis.Serum Gd-IgAl level in IgAN patients significantly increased,but serum Gd-IgAl may not directly mediate macrophages,cause disease progression and renal fibrosis. |
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