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构建用于预测糖尿病肾病风险的代谢-免疫模型及肠道微生物群研究

Construction of a metabolic-immune model for predicting the risk of diabetic nephropathy and study of gut microbiota.

作者信息

Dai Mengting, Wu Jianbo, Ji Zhaoyang, Chen Ping, Yang Chengchen, Luo Jialu, Shan Pengfei, Xu Mingzhi

机构信息

Zhejiang University of Medicine, Hangzhou, Zhejiang, China.

Department of Endocrinology and Metabolic Disease, Shulan (Hangzhou) Hospital Affiliated to Zhejiang Shuren University Shulan International Medical College, Hangzhou, Zhejiang, China.

出版信息

J Diabetes Investig. 2025 May;16(5):863-873. doi: 10.1111/jdi.14401. Epub 2025 Mar 3.

DOI:10.1111/jdi.14401
PMID:40029758
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12057383/
Abstract

AIMS

This study conducts a comprehensive analysis of the relative impact of risk factors for diabetic nephropathy (DN) during disease progression, with a particular emphasis on the role of gut microbiota. We developed multiple predictive models trying to enhance the early identification of high-risk patients in clinical practice.

MATERIALS AND METHODS

We collected data from type 2 diabetes mellitus patients, categorizing them by renal function for comparison. Logistic regression identified risk factors for DN, and we developed nomogram and random forest risk prediction models. Finally, we analyzed the correlations among these factors.

RESULTS

Compared to patients with diabetes alone, those with DN have a longer disease duration, characterized by abdominal obesity, hypertension, chronic inflammation, activation of the complement system, and declining renal function, along with a significant reduction in Bifidobacterium and Enterobacterium. Patients with macroalbuminuria exhibit a higher male prevalence, as well as elevated blood pressure and lipid levels, and poorer renal function. Increased waist-to-hip ratio, systolic blood pressure, urea, neutrophil-to-lymphocyte ratio, and complement C3, along with decreased Enterobacterium and albumin, have been identified as significant risk factors for DN. The nomogram model developed based on these findings demonstrates good predictive capacity. And the establishment of the random forest model further underscores the importance of the aforementioned indicators. Additionally, significant correlations were observed among obesity, inflammation, blood pressure, lipid levels, and gut microbiota.

CONCLUSIONS

Dysbiosis, metabolic disorders, and chronic inflammation play key roles in the progression of DN and may serve as new targets for future prevention and treatment strategies.

摘要

目的

本研究对糖尿病肾病(DN)疾病进展过程中危险因素的相对影响进行了全面分析,特别强调了肠道微生物群的作用。我们开发了多个预测模型,试图在临床实践中加强对高危患者的早期识别。

材料与方法

我们收集了2型糖尿病患者的数据,并根据肾功能对他们进行分类以作比较。逻辑回归确定了DN的危险因素,我们开发了列线图和随机森林风险预测模型。最后,我们分析了这些因素之间的相关性。

结果

与单纯糖尿病患者相比,DN患者病程更长,其特征为腹型肥胖、高血压、慢性炎症、补体系统激活以及肾功能下降,同时双歧杆菌和肠杆菌显著减少。大量白蛋白尿患者男性患病率更高,血压和血脂水平升高,肾功能较差。腰臀比增加、收缩压升高、尿素升高、中性粒细胞与淋巴细胞比值升高以及补体C3升高,同时肠杆菌和白蛋白减少,已被确定为DN的重要危险因素。基于这些发现开发的列线图模型显示出良好的预测能力。随机森林模型的建立进一步强调了上述指标的重要性。此外,在肥胖、炎症、血压、血脂水平和肠道微生物群之间观察到显著相关性。

结论

生态失调、代谢紊乱和慢性炎症在DN的进展中起关键作用,可能成为未来预防和治疗策略的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/baffc9034fb4/JDI-16-863-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/67fd174a460e/JDI-16-863-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/5bb0fb68bbf3/JDI-16-863-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/42676967f1a4/JDI-16-863-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/20ed521e2af7/JDI-16-863-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/5fe14ebd7a2b/JDI-16-863-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/baffc9034fb4/JDI-16-863-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/67fd174a460e/JDI-16-863-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/5bb0fb68bbf3/JDI-16-863-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/42676967f1a4/JDI-16-863-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/20ed521e2af7/JDI-16-863-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/5fe14ebd7a2b/JDI-16-863-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4919/12057383/baffc9034fb4/JDI-16-863-g005.jpg

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