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慢性肾脏病中的全身免疫炎症指数与死亡率

Systemic immune inflammatory index and mortality in chronic kidney disease.

作者信息

Ma Yanshuang, Yu Yang, Jia Zhongdan, Wang Hushan, Sun Mingli

机构信息

Department of Hyperbaric Oxygen, First Hospital of Jilin University, Changchun, Jilin, China.

Department of Anesthesiology, First Hospital of Jilin University, Changchun, Jilin, China.

出版信息

Front Endocrinol (Lausanne). 2025 Sep 3;16:1605543. doi: 10.3389/fendo.2025.1605543. eCollection 2025.

DOI:10.3389/fendo.2025.1605543
PMID:40969364
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12442490/
Abstract

BACKGROUND

Chronic kidney disease (CKD) is common and linked to higher mortality rates, but its relationship with the systemic immunoinflammatory index (SII) remains unclear, highlighting the need for further research.

METHODS

The SII is calculated by multiplying the counts of platelets and neutrophils, followed by dividing that product by the lymphocyte count. A diagnosis of CKD is made when the estimated glomerular filtration rate (eGFR) is below 60 mL/min/1.73 m². To further analyze the data, a multivariable Cox regression analysis, along with subgroup assessments, was performed. Analysis of survival data and threshold effects suggests that SII is a crucial independent factor related to mortality from all causes and cardiovascular issues in individuals with chronic kidney disease.

RESULTS

The study comprised a total of 46,620 individuals, with a weighted average age (standard error) of 47.00 (0.18) years. Among individuals over 20 years old suffering from CKD, the log-transformed SII demonstrated a nonlinear relationship, revealing a U-shaped correlation with the mortality rates associated with all causes as well as cardiovascular diseases (CVD). When SII.log as the log values rise, the likelihood of dying from all causes and cardiovascular issues initially shows a decline. Nevertheless, this pattern shifts, leading to an increased risk of mortality once a certain limit is surpassed. The evaluation of threshold impacts identified important levels starting at 6.06 and 6.25, which corresponded to the lowest observed mortality risk when evaluated through the SII.log values. The likelihood of mortality from all causes escalated once these limits were surpassed (HR 0.75, 95% CI 0.64-0.88; HR 1.74, 95% CI 1.55-1.95). The likelihood of mortality due to CVD also elevated (HR 1.01, 95% CI 0.78-1.31; HR 1.91, 95% CI 1.50-2.44). Higher SII levels correlated with decreased survival and longevity. In CKD patients over 45 years, SII reliably predicted all-cause mortality (statistically significant) and was linked to cardiovascular and cancer deaths (not statistically significant).

CONCLUSIONS

SII is an easily obtainable marker that may predict mortality in CKD patients over 45. More longitudinal research is needed to confirm its link with mortality rates (all causes, cardiovascular, and cancer) due to current limitations.

摘要

背景

慢性肾脏病(CKD)很常见,且与较高的死亡率相关,但其与全身免疫炎症指数(SII)的关系仍不清楚,这凸显了进一步研究的必要性。

方法

SII通过将血小板计数与中性粒细胞计数相乘,然后将该乘积除以淋巴细胞计数来计算。当估计肾小球滤过率(eGFR)低于60 mL/min/1.73 m²时,可诊断为CKD。为了进一步分析数据,进行了多变量Cox回归分析以及亚组评估。生存数据分析和阈值效应表明,SII是与慢性肾脏病患者全因死亡率和心血管问题相关的关键独立因素。

结果

该研究共纳入46,620名个体,加权平均年龄(标准误)为47.00(0.18)岁。在20岁以上的CKD患者中,对数转换后的SII呈现非线性关系,与全因死亡率以及心血管疾病(CVD)的死亡率呈U形相关性。当SII.log(对数形式的SII)值升高时,全因死亡和心血管疾病死亡的可能性最初呈下降趋势。然而,这种模式会发生变化,一旦超过某个限度,死亡风险就会增加。阈值影响评估确定了从6.06和6.25开始的重要水平,通过SII.log值评估时,这些水平对应着观察到的最低死亡风险。一旦超过这些限度,全因死亡的可能性就会上升(风险比[HR]为0.75,95%置信区间[CI]为0.64 - 0.88;HR为1.74,95% CI为1.55 - 1.95)。CVD导致的死亡可能性也会升高(HR为1.01,95% CI为0.78 - 1.31;HR为1.91,95% CI为1.50 - 2.44)。较高的SII水平与生存率降低和寿命缩短相关。在45岁以上的CKD患者中,SII能够可靠地预测全因死亡率(具有统计学意义),并且与心血管和癌症死亡相关(无统计学意义)。

结论

SII是一种易于获取的标志物,可能预测45岁以上CKD患者的死亡率。由于目前存在局限性,需要更多的纵向研究来证实其与死亡率(全因、心血管和癌症)的关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f26/12442490/7d3a67fefb7c/fendo-16-1605543-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f26/12442490/6976ab6a59a0/fendo-16-1605543-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f26/12442490/a0a844697e0f/fendo-16-1605543-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f26/12442490/7d3a67fefb7c/fendo-16-1605543-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f26/12442490/6976ab6a59a0/fendo-16-1605543-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f26/12442490/a0a844697e0f/fendo-16-1605543-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f26/12442490/7d3a67fefb7c/fendo-16-1605543-g003.jpg

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