Abstract
ObjectiveTo analyze the expression of macrophages, AIM, TGF-β1 in the kidney of IgAN patients, and to explore the role of macrophages, AIM, TGF-β1 in the progression of renal fibrosis in IgAN patients.MethodsThe paraffin specimens of renal tissue from 40 IgAN patients were selected as the observation group. At the same time, paraffin specimens of normal renal tissue from 11 patients treated by nephrectomy were selected as the normal control group. We observed the distribution of macrophages, the expression of AIM and TGF-β1 by immunohistochemical staining and/or immunofluorescence.ResultThe number of M0, M1, M2 macrophages could be found increased in IgAN patients. M0 macrophages are mainly polarized towards M2 macrophages. The expression of AIM and TGF-β1 were significantly higher in IgAN patients than in NC. M2 macrophage, AIM and TGF-β1 were positively correlated with serum creatinine and 24-hour proteinuria, but negatively correlated with eGFR. M2 macrophages, AIM, TGF-β1 were positively correlated with fibrotic area.ConclusionM2 macrophages, AIM and TGF-β1 play important roles in the process of IgAN fibrosis, and the three influence each other.
Highlights
IgA nephropathy (IgAN) is a common systemic immune glomerulonephritis, which is characterized by the deposition of IgA or IgA-based immune complexes in the mesangial region with mesangial cell proliferation and mesangial matrix expansion [1, 2]
Immunofluorescence and immunohistochemistry (Figures 1, 2) showed that macrophages in the IgAN group were mainly distributed in the renal tubular interstitial, and occasionally in the glomerular capillary plexus and renal tubular lumen, while macrophages were not distributed in normal renal tissue
Expression of Apoptosis inhibitor of macrophage (AIM), transforming growth factor-b1 (TGF-b1) in Renal Tissue In IgAN group, AIM mainly expressed in glomerular capillary loops and renal tubular epithelial cells, as well as in renal tubular lumen; TGF-b1 expressed mainly in renal tubular epithelial cells, and in renal interstitium
Summary
IgA nephropathy (IgAN) is a common systemic immune glomerulonephritis, which is characterized by the deposition of IgA or IgA-based immune complexes in the mesangial region with mesangial cell proliferation and mesangial matrix expansion [1, 2]. IgAN progresses slowly, up to 50% of patients develop to end-stage, and it is the main type that causes ESRD [3]. Renal fibrosis is the common pathway in the progression of chronic kidney disease (CKD) [4]. It is found that macrophages, Apoptosis inhibitor of macrophage (AIM) and transforming growth factor-b1 (TGF-b1) all play important roles in renal fibrosis. Macrophages are involved in the development of many kidney diseases. Some scholars believe that the deposition of macrophages in the kidney can be used as an important indicator to judge the development and prognosis of renal diseases.
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