Department of Family Medicine, Korean University Anam Hospital, 73 Goryeodae-ro, Seongbuk-gu, Seoul 02481, Republic of Korea (Dr Yoon).
Health-IT Center, Yonsei University Severance Hospital, Seoul, 03722, Republic of Korea (Dr Han).
J Clin Lipidol. 2024 Mar-Apr;18(2):e251-e260. doi: 10.1016/j.jacl.2024.01.002. Epub 2024 Jan 10.
There remains a limited comprehensive understanding of how dyslipidemia and chronic inflammation collectively contribute to the development of chronic kidney disease (CKD).
We aimed to identify clusters of individuals with five variables, including lipid profiles and C-reactive protein (CRP) levels, and to assess whether the clusters were associated with incident CKD risk.
We used the Korean Genome and Epidemiology Study-Ansan and Ansung data. K-means clustering analysis was performed to identify distinct clusters based on total cholesterol, triglyceride, non-high-density lipoprotein (HDL)-C, HDL-C, and CRP levels. Cox proportional hazards models were used to examine the association between incident CKD risk and the different clusters.
During the mean 10-year follow-up period, CKD developed in 1,645 participants (690 men and 955 women) among a total of 8,053 participants with a mean age of 51.8 years. Four distinct clusters were identified: C1, low cholesterol group (LC); C2, high-density lipoprotein cholesterol group (HC); C3, insulin resistance and inflammation group (IIC); and C4, dyslipidemia and inflammation group (DIC). Cluster 4 had a significantly higher risk of incident CKD compared to clusters 2 (hazard ratio (HR) 1.455 [95% confidence interval (CI) 1.234-1.715]; p < 0.001) and cluster 1 (HR 1.264 [95% CI 1.067-1.498]; p = 0.007) after adjusting for confounders. Cluster 3 had a significantly higher risk of incident CKD compared to clusters 2 and 1.
Clusters 4 and 3 had higher risk of incident CKD compared to clusters 2 and 1. The combination of dyslipidemia with inflammation or insulin resistance with inflammation appears to be pivotal in the development of incident CKD.
人们对血脂异常和慢性炎症如何共同导致慢性肾脏病(CKD)的发展仍缺乏全面的认识。
本研究旨在识别五个变量(包括血脂谱和 C 反应蛋白(CRP)水平)的个体聚类,并评估这些聚类与 CKD 发病风险是否相关。
我们使用了韩国基因组和流行病学研究-安山和安城的数据。采用 K 均值聚类分析,根据总胆固醇、甘油三酯、非高密度脂蛋白(HDL)-C、HDL-C 和 CRP 水平,确定不同的聚类。采用 Cox 比例风险模型评估不同聚类与 CKD 发病风险的关系。
在平均 10 年的随访期间,在总共 8053 名参与者中,有 1645 名(690 名男性和 955 名女性)发生了 CKD,参与者的平均年龄为 51.8 岁。确定了四个不同的聚类:C1,低胆固醇组(LC);C2,高密度脂蛋白胆固醇组(HC);C3,胰岛素抵抗和炎症组(IIC);C4,血脂异常和炎症组(DIC)。与聚类 2(危险比(HR)1.455[95%置信区间(CI)1.234-1.715];p<0.001)和聚类 1(HR 1.264[95% CI 1.067-1.498];p=0.007)相比,聚类 4 发生 CKD 的风险显著更高,调整混杂因素后。与聚类 2 和聚类 1 相比,聚类 3 发生 CKD 的风险显著更高。
与聚类 2 和聚类 1 相比,聚类 4 和聚类 3 发生 CKD 的风险更高。血脂异常与炎症或胰岛素抵抗与炎症的结合似乎在 CKD 的发生发展中起着关键作用。