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<title cf:type="text"><![CDATA[《中国临床新医学》杂志编辑部 -->Special Topic on Diagnosis and Treatment of Chronic Kidney Diseases]]></title>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Expression and significance of glomerular galactose-deficient IgA1 in glomerular disease characterized by abnormal deposition of IgA]]></title>
<link><![CDATA[https://www.zglcxyxzz.com/zglcxyyen/ch/reader/view_abstract.aspx?file_no=20240802&flag=1]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>［Abstract］　Objective</b>　To explore the expression and significance of glomerular galactose-deficient IgA1(Gd-IgA1) in glomerular disease characterized by abnormal deposition of IgA. <b>Methods</b>　Thirty-five patients with glomerular disease characterized by abnormal deposition of IgA who were admitted to Tianjin Medical University General Hospital from January 2020 to June 2024 were included as the IgA abnormal deposition group, including 5 cases of IgA-dominant infection-related glomerulonephritis(IgA-IRGN), 8 cases of diabetic nephropathy with IgA deposition(IgA-DN), 9 cases of anti-neutrophil cytoplasmic antibodies(ANCA)-associated glomerulonephritis with IgA deposition(IgA-ANCA-GN), and 13 cases of minimal change disease with IgA deposition(IgA-MCD). Other 35 sex- and age-matched primary IgA nephropathy(IgAN) patients hospitalized during the same period were selected as the controls(IgAN group). The clinical and pathological features of the patients in the two groups were analyzed, and the intensity and distribution characteristics of Gd-IgA1 staining in glomeruli in renal biopsy were evaluated. <b>Results</b>　The main clinical manifestations of the patients in the two groups were proteinuria and(or) hematuria, and elevated levels of blood creatinine. The results of renal pathological examination showed that endocapillary proliferation was more common in the patients in the IgAN group, while fibrinoid necrosis, crescent formation and basement membrane thickening were more common in the patients in the IgA abnormal deposition group. The results of immunohistochemical staining of Gd-IgA1 antibody KM55 showed that  KM55 was mainly expressed in the mesangial region in the IgAN group, and the staining intensity ranged from mildly positive(+) to strongly positive(+++), and the staining intensity in the patients of the IgAN group was significantly higher than that in the patients of the IgA abnormal deposition group(<i>P</i><0.05). The results of electron microscopy examination showed that the location of electron-dense deposits(EDD) in the glomeruli of the IgAN group was consistent with the IgA immunofluorescence and the KM55 staining. The location of glomerular EDD in the IgA abnormal deposition group was consistent with the IgA immunofluorescence staining, but was poorly consistent with the KM55 staining. <b>Conclusion</b>　In the glomerular disease characterized by abnormal deposition of IgA, glomerular Gd-IgA1 deposition is significantly less than glomerular IgA deposition, which suggests that Gd-IgA1 may not play an important role in its pathogenesis.]]></description>
<pubDate>2024/8/30 10:29:45</pubDate>
<category><![CDATA[Special Topic on Diagnosis and Treatment of Chronic Kidney Diseases]]></category>
<author><![CDATA[WANG Fanghao, SHANG Wenya, LI Hongfen, LIU Youxia, XING Yue, WU Zhanfei, LI Wenying, WEI Li, CHEN Jinju, JIA Junya]]></author>
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<atom:name>WANG Fanghao, SHANG Wenya, LI Hongfen, LIU Youxia, XING Yue, WU Zhanfei, LI Wenying, WEI Li, CHEN Jinju, JIA Junya</atom:name>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Study on the mechanism of action of miR-155 regulating the polarization of macrophages and mediating <br>podocyte injury through exosomes]]></title>
<link><![CDATA[https://www.zglcxyxzz.com/zglcxyyen/ch/reader/view_abstract.aspx?file_no=20240803&flag=1]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>［Abstract］　Objective</b>　To explore the mechanism of action of micro ribonucleic acid-155(miR-155) regulating the polarization of macrophages and mediating podocyte injury through exosomes. <b>Methods</b>　Macrophage RAW264.7 and glomerular podocyte MPC5 were selected for the experiments. The miR-155 mimics, miR-155 mimics negative control(NC), miR-155 inhibitor and miR-155 inhibitor NC lentiviruses were transfected into RAW264.7 cells, and miR-155 overexpressing/underexpressing macrophage cell lines and their controls were constructed and the macrophage exosomes were isolated. Macrophage M1/M2 phenotype ratio in each group was detected by using flow cytometry. RAW264.7 cells were co-cultured with MPC5 cells by using Transwell method, and the miR-155 expression level of macrophages was detected by using real-time fluorescence quantitative polymerase chain reaction(RT-qPCR) after 12 hours and 24 hours of co-culture, respectively, and the expression levels of interleukin(IL)-6 and IL-10 in macrophages, as well as the expression levels of synaptoporin and nephrin in glomerular podocytes were detected by using Western blot. The expression levels of IL-1β and IL-10 in glomerular podocytes were detected by using enzyme-linked immunosorbent assay(ELISA), and the apoptosis of glomerular podocytes was detected by using TUNEL staining method. <b>Results</b>　The miR-155 overexpressing/underexpressing macrophage cell lines were successfully constructed and their exosomes were successfully isolated. Overexpression of miR-155 could induce the polarization of macrophages to M1 type, and inhibition of miR-155 could induce the polarization of macrophages to M2 type. After miR-155 mimics lentiviruses were transfected into macrophages for 24 hours, their miR-155 expression levels were significantly increased(<i>P</i><0.05),  and the expression levels of IL-6 were up-regulated(<i>P</i><0.05), and  the expression levels of IL-10 were inhibited(<i>P</i><0.05), and the co-culture by using Transwell resulted in decrease in the expression levels of synaptoprin and nephrin in podocytes(<i>P</i><0.05), and increase in the expression level of IL-1β and facilitated podocyte apoptosis. However, the trend of the results obtained after transfection of miR-155 inhibitor lentiviruses into macrophages was opposite to that of miR-155 mimics. The results of RT-qPCR detection showed that the level of miR-155 in macrophage exosomes was significantly increased in the miR-155 mimics group(<i>P</i><0.05), and the level of miR-155 in macrophage exosomes in the miR-155 inhibitor group was significantly decreased(<i>P</i><0.05). <b>Conclusion</b>　Overexpression of miR-155 can induce macrophages to polarize into M1 type and induce podocyte injury mediated by exosomes, while downregulation of miR-155 expression reverses this effect.]]></description>
<pubDate>2024/8/30 0:00:00</pubDate>
<category><![CDATA[Special Topic on Diagnosis and Treatment of Chronic Kidney Diseases]]></category>
<author><![CDATA[XU Luyao<sup>1,2</sup>, ZHANG Jie<sup>1,2</sup>, LIN Xu<sup>2,3</sup>]]></author>
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<atom:name>XU Luyao<sup>1,2</sup>, ZHANG Jie<sup>1,2</sup>, LIN Xu<sup>2,3</sup></atom:name>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[The association between <i>mTOR</i> gene polymorphism and antineutrophil cytoplasmic antibody-associated vasculitis in a population of Guangxi]]></title>
<link><![CDATA[https://www.zglcxyxzz.com/zglcxyyen/ch/reader/view_abstract.aspx?file_no=20240804&flag=1]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>［Abstract］　Objective</b>　To explore the association between single-nucleotide polymorphism(SNP) of rs4845856 locus in mammalian target of rapamycin(<i>mTOR</i>) gene and antineutrophil cytoplasmic antibody(ANCA)-associated vasculitis(AAV) in a population of Guangxi. <b>Methods</b>　A total of 212 outpatients who were made a definite diagnosis with AAV in the Second Affiliated Hospital of Guangxi Medical University and Wuzhou Gongren Hospital from 2005 to 2022 were included as AAV group and 208 healthy examinees were selected as control group during the same period. Multiple polymerase chain reaction combined with high-throughput sequencing were employed to perform genotyping detection on the selected loci. The gene frequency and genotype distribution were compared between the two groups. The relationship between gene polymorphism and the risk of the occurrence of AAV was analyzed through genetic modeling, and a comparative analysis was conducted based on the clinical data of the AAV group. <b>Results</b>　There was no significant difference in genotype frequency and allele frequency distribution of rs4845856 locus between the two groups(<i>P</i>>0.05). For the female subgroup, in the co-dominant model［<i>OR</i>(95%<i>CI</i>): 0.11(0.01-0.86), <i>P</i>=0.005］ and the recessive model［<i>OR</i>(95%<i>CI</i>): 0.09(0.01-0.75), <i>P</i>=0.003］, the TT genotype showed a strong association with AAV susceptibility and was considered as a protective factor for the occurrence of AAV. For the Han nationality subgroup, there was also an association between TT genotype and AAV susceptibility in the recessive model［<i>OR</i>(95%<i>CI</i>): 0.29(0.08-1.05), <i>P</i>=0.038］. Proteinase 3(PR3) and myeloperoxidase(MPO) were associated with various genotypes of SNP of rs4845856 locus(<i>P</i><0.05). In the AAV group, there were no associations between the genotypes of SNP of rs4845856 locus and the pathological types(<i>P</i>>0.05). <b>Conclusion</b>　The SNP of rs4845856 locus in <i>mTOR</i> gene might be associated with genetic susceptibility to AAV in the population of Guangxi. The TT genotype may be an important protective factor in the female subpopulation.]]></description>
<pubDate>2024/8/30 0:00:00</pubDate>
<category><![CDATA[Special Topic on Diagnosis and Treatment of Chronic Kidney Diseases]]></category>
<author><![CDATA[SU Shan<sup>1</sup>, XUE Chao<sup>2</sup>, QIU Chenggao<sup>1</sup>]]></author>
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<atom:name>SU Shan<sup>1</sup>, XUE Chao<sup>2</sup>, QIU Chenggao<sup>1</sup></atom:name>
</atom:author>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Research progress of hypoxia-inducible factor-prolyl hydroxylase inhibitor in vascular calcification in chronic kidney disease]]></title>
<link><![CDATA[https://www.zglcxyxzz.com/zglcxyyen/ch/reader/view_abstract.aspx?file_no=20240805&flag=1]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>［Abstract］</b>　Hypoxia-inducible factor-prolyl hydroxylase inhibitor(HIF-PHI) is a novel drug for treating renal anemia in chronic kidney disease(CKD). As a stabilizer of hypoxia-inducible factor(HIF), HIF-PHI can increase the expression level of HIF, and the continuous increase of HIF can promote the osteogenic transdifferentiation and calcification of vascular smooth muscle cells, which has the risk of increasing vascular calcification. Long-term use of HIF-PHI may have the potential risk of vascular calcification. Vascular calcification is a major risk factor for the increase of incidence rate and mortality rate of cardiovascular events in CKD patients. Therefore, the potential hazards of HIF-PHI should be fully understood and taken seriously. This paper reviews the research progress of HIF-PHI in vascular calcification in CKD.]]></description>
<pubDate>2024/8/30 10:29:46</pubDate>
<category><![CDATA[Special Topic on Diagnosis and Treatment of Chronic Kidney Diseases]]></category>
<author><![CDATA[LI Lin, YOU Yanwu]]></author>
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<atom:name>LI Lin, YOU Yanwu</atom:name>
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