{"title":"临床试验:自体树突状细胞给药对糖尿病肾病肾脏血流动力学和炎症生物标志物的影响。","authors":"Endang Drajat, Aziza Ghanie Icksan, Jonny Jonny, Aditya Pratama Lokeswara, Bhimo Aji Hernowo, Elvita Rahmi Daulay, Terawan Agus Putranto","doi":"10.3390/diseases13040122","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Diabetic kidney disease (DKD) is a significant risk factor for End-Stage Renal Disease, with a high global incidence and mortality rate. Hyperglycemia in DKD induces inflammation, contributing to glomerular hyperfiltration, fibrosis, and impaired renal function. Current therapies, including SGLT2 inhibitors, ACE inhibitors, and ARBs, show limited efficacy. Autologous dendritic cells (DCs) offer potential anti-inflammatory effects by reducing cytokine activity and fibrosis biomarkers.</p><p><strong>Methods: </strong>A quasi-experimental pretest-post-test design was conducted involving 29 DKD patients. Baseline blood and urine samples were collected for MMP-9, TGF-β, and Doppler ultrasound (PSV, EDV) measurements. The subjects received subcutaneous injections of autologous DCs, and follow-up measurements were conducted four weeks after treatment. The statistical analyses included paired t-tests, Wilcoxon signed-rank tests, and linear regression.</p><p><strong>Results: </strong>After treatment, there were a significant decrease in PSV (from 47.1 ± 23.87 cm/s to 27.85 ± 20.53 cm/s, <i>p</i> = 0.044) and a significant increase in EDV (from 13 ± 5.32 cm/s to 15.7 ± 12.55 cm/s, <i>p</i> = 0.039). A strong correlation was observed between the TGF-β and MMP-9 levels (<i>p</i> = 0.001). Linear regression analysis showed reduced MMP-9 influence on the TGF-β after treatment, suggesting potential fibrosis reduction. Gender and UACR subgroup analyses revealed significant PSV and EDV improvements in females and the microalbuminuria group.</p><p><strong>Conclusion: </strong>Autologous dendritic cell therapy significantly improved renal hemodynamics and showed potential to reduce fibrosis by modulating TGF-β and MMP-9 levels in DKD patients, warranting further investigation.</p>","PeriodicalId":72832,"journal":{"name":"Diseases (Basel, Switzerland)","volume":"13 4","pages":""},"PeriodicalIF":3.0000,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12025661/pdf/","citationCount":"0","resultStr":"{\"title\":\"Clinical Trial: Effects of Autologous Dendritic Cell Administration on Renal Hemodynamics and Inflammatory Biomarkers in Diabetic Kidney Disease.\",\"authors\":\"Endang Drajat, Aziza Ghanie Icksan, Jonny Jonny, Aditya Pratama Lokeswara, Bhimo Aji Hernowo, Elvita Rahmi Daulay, Terawan Agus Putranto\",\"doi\":\"10.3390/diseases13040122\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Diabetic kidney disease (DKD) is a significant risk factor for End-Stage Renal Disease, with a high global incidence and mortality rate. Hyperglycemia in DKD induces inflammation, contributing to glomerular hyperfiltration, fibrosis, and impaired renal function. Current therapies, including SGLT2 inhibitors, ACE inhibitors, and ARBs, show limited efficacy. Autologous dendritic cells (DCs) offer potential anti-inflammatory effects by reducing cytokine activity and fibrosis biomarkers.</p><p><strong>Methods: </strong>A quasi-experimental pretest-post-test design was conducted involving 29 DKD patients. Baseline blood and urine samples were collected for MMP-9, TGF-β, and Doppler ultrasound (PSV, EDV) measurements. The subjects received subcutaneous injections of autologous DCs, and follow-up measurements were conducted four weeks after treatment. The statistical analyses included paired t-tests, Wilcoxon signed-rank tests, and linear regression.</p><p><strong>Results: </strong>After treatment, there were a significant decrease in PSV (from 47.1 ± 23.87 cm/s to 27.85 ± 20.53 cm/s, <i>p</i> = 0.044) and a significant increase in EDV (from 13 ± 5.32 cm/s to 15.7 ± 12.55 cm/s, <i>p</i> = 0.039). A strong correlation was observed between the TGF-β and MMP-9 levels (<i>p</i> = 0.001). Linear regression analysis showed reduced MMP-9 influence on the TGF-β after treatment, suggesting potential fibrosis reduction. Gender and UACR subgroup analyses revealed significant PSV and EDV improvements in females and the microalbuminuria group.</p><p><strong>Conclusion: </strong>Autologous dendritic cell therapy significantly improved renal hemodynamics and showed potential to reduce fibrosis by modulating TGF-β and MMP-9 levels in DKD patients, warranting further investigation.</p>\",\"PeriodicalId\":72832,\"journal\":{\"name\":\"Diseases (Basel, Switzerland)\",\"volume\":\"13 4\",\"pages\":\"\"},\"PeriodicalIF\":3.0000,\"publicationDate\":\"2025-04-21\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12025661/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Diseases (Basel, Switzerland)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3390/diseases13040122\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Diseases (Basel, Switzerland)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3390/diseases13040122","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
摘要
背景:糖尿病肾病(DKD)是终末期肾病的重要危险因素,全球发病率和死亡率都很高。DKD的高血糖会引起炎症,导致肾小球过滤、纤维化和肾功能受损。目前的治疗方法,包括SGLT2抑制剂、ACE抑制剂和arb,显示出有限的疗效。自体树突状细胞(dc)通过降低细胞因子活性和纤维化生物标志物提供潜在的抗炎作用。方法:29例DKD患者采用准实验前测后测设计。收集基线血液和尿液样本进行MMP-9、TGF-β和多普勒超声(PSV、EDV)测量。受试者接受自体dc皮下注射,治疗后4周进行随访测量。统计分析包括配对t检验、Wilcoxon符号秩检验和线性回归。结果:治疗后PSV由47.1±23.87 cm/s降至27.85±20.53 cm/s, p = 0.044; EDV由13±5.32 cm/s降至15.7±12.55 cm/s, p = 0.039;TGF-β与MMP-9水平有显著相关性(p = 0.001)。线性回归分析显示,治疗后MMP-9对TGF-β的影响降低,提示潜在的纤维化减轻。性别和UACR亚组分析显示,女性和微量白蛋白尿组PSV和EDV显著改善。结论:自体树突状细胞治疗可显著改善肾脏血流动力学,并通过调节DKD患者TGF-β和MMP-9水平,显示出减少纤维化的潜力,值得进一步研究。
Clinical Trial: Effects of Autologous Dendritic Cell Administration on Renal Hemodynamics and Inflammatory Biomarkers in Diabetic Kidney Disease.
Background: Diabetic kidney disease (DKD) is a significant risk factor for End-Stage Renal Disease, with a high global incidence and mortality rate. Hyperglycemia in DKD induces inflammation, contributing to glomerular hyperfiltration, fibrosis, and impaired renal function. Current therapies, including SGLT2 inhibitors, ACE inhibitors, and ARBs, show limited efficacy. Autologous dendritic cells (DCs) offer potential anti-inflammatory effects by reducing cytokine activity and fibrosis biomarkers.
Methods: A quasi-experimental pretest-post-test design was conducted involving 29 DKD patients. Baseline blood and urine samples were collected for MMP-9, TGF-β, and Doppler ultrasound (PSV, EDV) measurements. The subjects received subcutaneous injections of autologous DCs, and follow-up measurements were conducted four weeks after treatment. The statistical analyses included paired t-tests, Wilcoxon signed-rank tests, and linear regression.
Results: After treatment, there were a significant decrease in PSV (from 47.1 ± 23.87 cm/s to 27.85 ± 20.53 cm/s, p = 0.044) and a significant increase in EDV (from 13 ± 5.32 cm/s to 15.7 ± 12.55 cm/s, p = 0.039). A strong correlation was observed between the TGF-β and MMP-9 levels (p = 0.001). Linear regression analysis showed reduced MMP-9 influence on the TGF-β after treatment, suggesting potential fibrosis reduction. Gender and UACR subgroup analyses revealed significant PSV and EDV improvements in females and the microalbuminuria group.
Conclusion: Autologous dendritic cell therapy significantly improved renal hemodynamics and showed potential to reduce fibrosis by modulating TGF-β and MMP-9 levels in DKD patients, warranting further investigation.