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<title cf:type="text"><![CDATA[《中国临床新医学》杂志编辑部 -->Special Topic on Prevention 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[Precision medicine for IgA nephropathy: frontiers in epidemiology and pathogenesis]]></title>
<link><![CDATA[https://www.zglcxyxzz.com/zglcxyyen/ch/reader/view_abstract.aspx?file_no=20251202&flag=1]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>［Abstract］</b>　Immunoglobulin A(IgA) nephropathy(IgAN), also known as Berger′s disease, is a glomerular disease characterized by the deposition of IgA or IgA immune complexes in the glomerular mesangial area. At present, IgAN is the most common primary glomerular disease worldwide. The characteristics of IgAN are complex due to differences in region, race, gender and age, suggesting that genetic and environmental factors play key roles in IgAN. In recent years, breakthroughs have been made in the research on the pathogenesis of IgAN in the aspects of immunology and molecular pathological mechanisms. The core link in the development of IgAN is the imbalance in the formation and clearance of the galactose-deficient immunoglobulin A1(Gd-IgA1) immune complex driven by mucosal immune dysregulation, resulting in IgA-specific deposition in the mesangial area and complement activation, which is the result of the interplay of genetic-environmental-immune factors. The hypothesis on anti-mesangial cell autoantibodies proposed in recent years has provided a new perspective for research on the etiology of IgAN. This paper systematically integrates the cutting-edge evidence on the epidemiology and pathogenesis of IgAN, providing a theoretical basis for the individualized treatment of IgAN.]]></description>
<pubDate>2025/12/31 13:19:40</pubDate>
<category><![CDATA[Special Topic on Prevention and Treatment of Chronic Kidney Diseases]]></category>
<author><![CDATA[ZHOU Ruijia, LIU Hong]]></author>
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<atom:name>ZHOU Ruijia, LIU Hong</atom:name>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Rho kinase signaling pathway mediates high uric acid-induced oxidative damage and apoptosis of renal tubular cells by regulating mitochondrial dynamin and biosynthesis related genes]]></title>
<link><![CDATA[https://www.zglcxyxzz.com/zglcxyyen/ch/reader/view_abstract.aspx?file_no=20251203&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 related mechanisms of oxidative damage and apoptosis of renal tubules in hyperuricemia mediated by the Rho kinase signaling pathway via the mitochondrial pathway. <b>Methods</b>　Human renal tubular epithelial cells(HK-2 cells) were divided into 6 groups: NC group(normal control), transforming growth factor-β1(TGF-β1) group, uric acid group(intervention with high uric acid stimulation), fasudil group［receiving Rho-associated protein kinase(ROCK) inhibitor］, ROCK1 siRNA group(intervention with <i>ROCK1</i> gene silencing), sc-siRNA group(negative control). The expression levels of mitochondrial-related proteins in the cells of each group were detected by using Western blot and quantitative real-time polymerase chain reaction(qRT-PCR), and the expression levels were compared among different groups. <b>Results</b>　High uric acid significantly upregulated the expression of myosin phosphatase-targeting subunit 1(MYPT1) in HK-2 cells, suggesting an increase in Rho kinase activity. High uric acid upregulated the expression level of manganese superoxide dismutase 2(MnSOD2) mRNA in HK-2 cells, while the pretreatment with fasudil significantly inhibited this change. After transfection with ROCK1 siRNA, the expression level of MnSOD2 mRNA in HK-2 cells was significantly decreased. The regulations of mitochondrial dynamin and biosynthesis genes via the Rho kinase pathway also affected the apoptosis process of the cells. <b>Conclusion</b>　Rho kinase may accelerate the progression of hyperuricemic nephropathy by regulating mitochondrial oxidative damage and apoptosis.]]></description>
<pubDate>2025/12/31 13:19:40</pubDate>
<category><![CDATA[Special Topic on Prevention and Treatment of Chronic Kidney Diseases]]></category>
<author><![CDATA[LI Jiachang<sup>1</sup>, MA Yuhan<sup>2</sup>, WEI Jiali<sup>1</sup>]]></author>
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<atom:name>LI Jiachang<sup>1</sup>, MA Yuhan<sup>2</sup>, WEI Jiali<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[Exploration on mechanism of action of nalfurafine in treatment of chronic kidney disease-associated pruritus based on network pharmacology and molecular docking techniques]]></title>
<link><![CDATA[https://www.zglcxyxzz.com/zglcxyyen/ch/reader/view_abstract.aspx?file_no=20251204&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 nalfurafine in treatment of chronic kidney disease-associated pruritus(CKD-aP) based on network pharmacology and molecular docking techniques. <b>Methods</b>　The basic information and target sites of nalfurafine were obtained via Chemical Book platform,  SwissTargetPrediction database and GeneCards database. Comparative Toxicogenomics Database(CTD) and GeneCards database were used to screen the target sites related to  chronic kidney disease(CKD) and pruritus. The data update of the relevant databases was up to July 2025. The protein-protein interaction(PPI) network was constructed. Gene Ontology(GO) function enrichment analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analysis were performed on the common target sites. <b>Results</b>　A total of 100 effect target genes of nalfurafine, 4 277 target genes related to CKD, 4 091 target genes related to pruritus, and 49 nalfurafine and CKD-aP common target genes were obtained. Nine key target genes were obtained through the screening of PPI network. A total of 933 enrichment results were obtained by using GO enrichment analysis, among which biological processes(BP) were mainly involved in phosphorylation, transmembrane receptor protein tyrosine kinase signal pathway and protein phosphorylation, and cellular components(CC) were mainly involved in receptor complex, postsynaptic portion and ⅠA phosphatidylinositol 3-kinase complex, and molecular functions(MF) were mainly involved in protein kinase activity, phosphotransferase activity with ethanol as receptor and kinase activity. A total of 139 pathways were obtained by using KEGG enrichment analysis, which were mainly involved in epidermal growth factor receptor(EGFR) tyrosine kinase inhibitor resistance, PI3K-Akt signal pathway and ErbB signal pathway. <b>Conclusion</b>　Nalfurafine can treat CKD-aP via multiple targets and pathways, which provides a theoretical basis for further research on nalfurafine.]]></description>
<pubDate>2025/12/31 13:19:40</pubDate>
<category><![CDATA[Special Topic on Prevention and Treatment of Chronic Kidney Diseases]]></category>
<author><![CDATA[LI Jing, SHI Jingxuan, WANG Xu, ZHANG Zheng, ZHUO Li, LI Wenge]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>LI Jing, SHI Jingxuan, WANG Xu, ZHANG Zheng, ZHUO Li, LI Wenge</atom:name>
</atom:author>
<guid><![CDATA[https://www.zglcxyxzz.com/zglcxyyen/ch/reader/view_abstract.aspx?file_no=20251204&flag=1]]></guid><cfi:id>3</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Artificial intelligence empowers kidney disease research: mechanism exploration and treatment optimization]]></title>
<link><![CDATA[https://www.zglcxyxzz.com/zglcxyyen/ch/reader/view_abstract.aspx?file_no=20251205&flag=1]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>［Abstract］</b>　Kidney diseases pose one of the major burdens on global public health, and their incidence and mortality continue to rise. The rapid development of artificial intelligence(AI) provides revolutionary tools for exploring the mechanisms of kidney diseases and optimizing clinical treatments. This review summarizes the main types of kidney diseases and their complex pathogenic mechanisms, and points out the limitations of traditional research methods, and elaborates on the applications of AI in multi-omics data analysis, pathological image recognition in kidney diseases, big data-driven risk prediction, and mechanism analysis of rare kidney diseases. In clinical treatments, AI assists early screening, optimizations of individualized nutrition and dialysis, management of prognosis, and kidney transplant matching, significantly improving diagnostic accuracy and patient prognosis. This review also analyzes the challenges faced by AI and looks forward to the future prospects of multimodal fusion, federated learning, and large language models in precision medicine for kidney diseases.]]></description>
<pubDate>2025/12/31 13:19:40</pubDate>
<category><![CDATA[Special Topic on Prevention and Treatment of Chronic Kidney Diseases]]></category>
<author><![CDATA[MENG Lingzhang<sup>1,2</sup>, YANG Mingyue<sup>1,2,3</sup>, XIONG Lijia<sup>1</sup>, WEI Suosu<sup>1</sup>, HUANG Xiaoyuan<sup>1</sup>, LIANG Huaqian<sup>1</sup>, MAO Xiuli<sup>1,2,4</sup>, ZHANG Xiamin<sup>1,2,4</sup>, LIN Wenxian<sup>1</sup>, YE Kun<sup>1</sup>]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>MENG Lingzhang<sup>1,2</sup>, YANG Mingyue<sup>1,2,3</sup>, XIONG Lijia<sup>1</sup>, WEI Suosu<sup>1</sup>, HUANG Xiaoyuan<sup>1</sup>, LIANG Huaqian<sup>1</sup>, MAO Xiuli<sup>1,2,4</sup>, ZHANG Xiamin<sup>1,2,4</sup>, LIN Wenxian<sup>1</sup>, YE Kun<sup>1</sup></atom:name>
</atom:author>
<guid><![CDATA[https://www.zglcxyxzz.com/zglcxyyen/ch/reader/view_abstract.aspx?file_no=20251205&flag=1]]></guid><cfi:id>2</cfi:id><cfi:read>true</cfi:read></item>
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<title xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="text"><![CDATA[Analysis on the efficacy and safety of rituximab in treatment of refractory primary focal segmental glomerulosclerosis in adults]]></title>
<link><![CDATA[https://www.zglcxyxzz.com/zglcxyyen/ch/reader/view_abstract.aspx?file_no=20251206&flag=1]]></link>
<description xmlns:cf="http://www.microsoft.com/schemas/rss/core/2005" cf:type="html"><![CDATA[<b>［Abstract］　Objective</b>　To analyze the efficacy and safety of rituximab(RTX) in treatment of refractory primary focal segmental glomerulosclerosis(FSGS) in adults. <b>Methods</b>　The clinical data of 14 adult patients who were diagnosed with refractory primary FSGS and received RTX treatment in Department of Nephrology, the People′s Hospital of Guangxi Zhuang Autonomous Region from January 1, 2021 to July 31, 2025 were retrospectively analyzed. These data were sourced from the electronic medical record system of the People′s Hospital of Guangxi Zhuang Autonomous Region and the follow-up records of the patients. <b>Results</b>　The pathological types included 12 cases of non-specific type and 2 cases of apical type. The median age of the patients receiving RTX treatment for the first time was 37.5(23.0, 69.5)years. Nine patients received single-dose treatment and 5 patients received 2-dose treatment, and the regular follow-up was completed in all the patients. At the 6-month follow-up, 9 patients achieved complete remission and 5 patients achieved partial remission. Three FSGS patients with steroid-resistant type achieved complete remission at the sixth month of RTX treatment. Three overweight patients and one obese patient were treated with a single dose of RTX and all of them achieved complete remission 6 months after RTX treatment. During the follow-up period, all the patients did not experience any drug-related adverse reactions. <b>Conclusion</b>　A single dose of RTX is not only effective for adult patients with steroid-dependent type and frequently relapsing type of FSGS, but also applicable to steroid-resistant type of FSGS. The therapeutic response to a single dose of RTX in overweight and obese patients may not be significantly different from that in normal-weight and underweight patients. After RTX treatment, the patients need to be closely followed up and attention should be paid to preventing infection in them.]]></description>
<pubDate>2025/12/31 13:19:40</pubDate>
<category><![CDATA[Special Topic on Prevention and Treatment of Chronic Kidney Diseases]]></category>
<author><![CDATA[GUAN Lisi<sup>1,2</sup>, YE Kun<sup>2,3</sup>, WEI Qiaoyu<sup>2,3</sup>, DENG Meiqiu<sup>2,3</sup>, HUANG Shaorong<sup>1,2</sup>]]></author>
<atom:author xmlns:atom="http://www.w3.org/2005/Atom">
<atom:name>GUAN Lisi<sup>1,2</sup>, YE Kun<sup>2,3</sup>, WEI Qiaoyu<sup>2,3</sup>, DENG Meiqiu<sup>2,3</sup>, HUANG Shaorong<sup>1,2</sup></atom:name>
</atom:author>
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