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糖尿病肾病患者全身免疫炎症指数与全因死亡率及心脑血管死亡率的关联:来自1999 - 2018年美国国家健康与营养检查调查(NHANES)的证据

Association of systemic immune-inflammation index with all-cause and cardio-cerebrovascular mortality in individuals with diabetic kidney disease: evidence from NHANES 1999-2018.

作者信息

Zhang Manhuai, Ye Siyang, Li Jianbo, Zhang Meng, Tan Li, Wang Yiqin, Xie Peichen, Peng Huajing, Li Suchun, Chen Sixiu, Wen Qiong, Chan Kam Wa, Tang Sydney C W, Li Bin, Chen Wei

机构信息

Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China.

出版信息

Front Endocrinol (Lausanne). 2024 Nov 26;15:1399832. doi: 10.3389/fendo.2024.1399832. eCollection 2024.

DOI:10.3389/fendo.2024.1399832
PMID:39659615
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11628304/
Abstract

BACKGROUND

Emerging evidence suggests a potential role of immune response and inflammation in the pathogenesis of diabetic kidney disease (DKD). The systemic immune-inflammation index (SII) offers a comprehensive measure of inflammation; however, its relationship with the prognosis of DKD patients remains unclear.

METHODS

Using data from the National Health and Nutrition Examination Survey (NHANES) spanning 1999 to 2018, this cross-sectional study involved adults diagnosed with DKD. Cox proportional hazards models were utilized to assess the associations between SII and all-cause or cardio-cerebrovascular disease mortality. Additionally, restricted cubic spline, piecewise linear regression, and subgroup analyses were performed.

RESULTS

Over a median follow-up duration of 6.16 years, 1338 all-cause deaths were recorded. After adjusting for covariates, elevated SII levels were significantly associated with increased risks of all-cause and cardio-cerebrovascular disease mortality. Specifically, per one-unit increment in natural log-transformed SII (lnSII), there was a 29% increased risk of all-cause mortality ( < 0.001) and a 23% increased risk of cardio-cerebrovascular disease mortality ( = 0.01) in the fully adjusted model. Similar results were observed when SII was analyzed as a categorical variable (quartiles). Moreover, nonlinear association was identified between SII and all-cause mortality ( < 0.001) through restricted cubic spline analysis, with threshold value of 5.82 for lnSII. The robustness of these findings was confirmed in subgroup analyses. Likewise, the statistically significant correlation between SII levels and cardio-cerebrovascular disease mortality persisted in individuals with DKD.

CONCLUSION

Increased SII levels, whether examined as continuous variables or categorized, demonstrate a significant association with elevated risks of all-cause and cardio-cerebrovascular disease mortality among DKD patients. These findings imply that maintaining SII within an optimal range could be crucial in reducing mortality risk.

摘要

背景

新出现的证据表明免疫反应和炎症在糖尿病肾病(DKD)发病机制中可能发挥作用。全身免疫炎症指数(SII)提供了一种全面的炎症测量方法;然而,其与DKD患者预后的关系仍不清楚。

方法

利用1999年至2018年美国国家健康与营养检查调查(NHANES)的数据,这项横断面研究纳入了被诊断为DKD的成年人。采用Cox比例风险模型评估SII与全因或心脑血管疾病死亡率之间的关联。此外,还进行了受限立方样条、分段线性回归和亚组分析。

结果

在中位随访时间6.16年期间,记录了1338例全因死亡。在调整协变量后,SII水平升高与全因和心脑血管疾病死亡风险增加显著相关。具体而言,在完全调整模型中,自然对数转换后的SII(lnSII)每增加一个单位,全因死亡风险增加29%(<0.001),心脑血管疾病死亡风险增加23%(=0.01)。将SII作为分类变量(四分位数)进行分析时,观察到类似结果。此外,通过受限立方样条分析确定SII与全因死亡率之间存在非线性关联(<0.001),lnSII的阈值为5.82。这些发现的稳健性在亚组分析中得到证实。同样,SII水平与心脑血管疾病死亡率之间的统计学显著相关性在DKD患者中持续存在。

结论

无论作为连续变量还是分类变量进行检查,SII水平升高均表明与DKD患者全因和心脑血管疾病死亡风险增加显著相关。这些发现意味着将SII维持在最佳范围内对于降低死亡风险可能至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24a/11628304/a7882bd90590/fendo-15-1399832-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24a/11628304/95294a1eadb0/fendo-15-1399832-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24a/11628304/680abc813dac/fendo-15-1399832-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24a/11628304/a7882bd90590/fendo-15-1399832-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24a/11628304/95294a1eadb0/fendo-15-1399832-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24a/11628304/680abc813dac/fendo-15-1399832-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24a/11628304/a7882bd90590/fendo-15-1399832-g003.jpg

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