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Background <p>The ratio of uric acid to high-density lipoprotein cholesterol (UHR) is a novel comprehensive indicator related to dyslipidemia. However, the association between UHR and coronary artery disease (CAD) risk in patients with chronic kidney disease (CKD) remains unclear.</p> Methods <p>After matching based on age and gender propensity scores, 2124 subjects were included and divided into the CKD group (708 cases) and the non-CKD group (1416 cases). The predictive performance of UHR for CAD was evaluated by the area under the curve (AUC), and the independent association between UHR and the risk of CAD onset was analyzed using a multivariate logistic regression model. The correlation and dose-response relationship between the ratio of uric acid to high-density lipoprotein cholesterol (UHR) and the risk of CAD were analyzed using LOESS fitting and restricted cubic spline (RCS) analysis.</p> Results <p>After matching, the multiple lipid-related indices (Triglycerides (TG), Remnant Cholesterol (RC), Atherogenic Index (AI), Atherogenic Index of Plasma (AIP), Triglyceride Glucose Index (TyG), Lipoprotein Composite Index (LCI), Triglyceride to High-Density Lipoprotein Cholesterol Ratio (TG/HDL-C), Total Cholesterol to High-Density Lipoprotein Cholesterol Ratio (TC/HDL-C), Low-Density Lipoprotein Cholesterol to High-Density Lipoprotein Cholesterol Ratio (LDL-C/HDL-C), UHR) in the CKD group were significantly higher than those in the non-CKD group. The AUC analysis showed that HDL-C, AIP, TG/HDL-C, and UHR had strong predictive performance in the overall cohort and the non-CKD group, while in the CKD group, HDL-C, AI, and TC/HDL-C are better predictive indicators. After adjusting for all confounding factors, multivariate regression analysis revealed that HDL-C, apolipoprotein A-1 (APOA-1), and the APOA-1/APOB ratio were independent protective factors for CAD in the entire cohort. Among them, the protective effect of HDL-C was the most stable (overall population aOR = 0.26, 95% CI: 0.17–0.39, <i>p</i> &lt; 0.001), and it was significantly in both the CKD (aOR = 0.18, 95% CI: 0.09–0.40, <i>p</i> &lt; 0.001) and non-CKD subgroups (aOR = 0.31, 95% CI: 0.18–0.52, <i>p</i> &lt; 0.001). In CKD, UHR is significantly correlated with CAD (aOR = 6.23, 95% CI: 1.89–20.60, <i>p</i> = 0.003), and the association was more significant in the non-CKD group (aOR = 15.15, 95% CI: 4.20–54.72, <i>p</i> &lt; 0.001). CKD status significantly modified the association between UHR and CAD (P for interaction = 0.015). LOESS fitting suggested that UHR was positively correlated with the probability of CAD occurrence (the correlation was more significant at low UHR, and it slowed down when UHR &gt; 0.5, <i>r</i> = 0.2, <i>p</i> &lt; 0.001), and negatively correlated with eGFR (<i>r</i> = -0.38, <i>p</i> &lt; 0.001). RCS analysis confirmed a significant nonlinear association between UHR and CAD (overall <i>P</i> &lt; 0.001, nonlinear <i>P</i> = 0.002), and the risk of CAD increased when UHR was &gt; 0.41 in CKD patients.</p> Conclusions <p>UHR is an independent risk factor for coronary heart disease, with higher adjusted OR values and more significant independent risk effects in non-CKD populations.</p>

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Association of uric acid-to-HDL cholesterol ratio and coronary atherosclerotic heart disease in patients with and without CKD

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月15日

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  • Chang-Hao Sun,
  • Xin-Yu Zhu,
  • Zhi-Long Wang,
  • Zhen-Lin Liu,
  • Xiao-Tong Wang,
  • Jin-Qiu Wei,
  • Teng-Teng Zhu,
  • Yong Zhang

摘要

Background

The ratio of uric acid to high-density lipoprotein cholesterol (UHR) is a novel comprehensive indicator related to dyslipidemia. However, the association between UHR and coronary artery disease (CAD) risk in patients with chronic kidney disease (CKD) remains unclear.

Methods

After matching based on age and gender propensity scores, 2124 subjects were included and divided into the CKD group (708 cases) and the non-CKD group (1416 cases). The predictive performance of UHR for CAD was evaluated by the area under the curve (AUC), and the independent association between UHR and the risk of CAD onset was analyzed using a multivariate logistic regression model. The correlation and dose-response relationship between the ratio of uric acid to high-density lipoprotein cholesterol (UHR) and the risk of CAD were analyzed using LOESS fitting and restricted cubic spline (RCS) analysis.

Results

After matching, the multiple lipid-related indices (Triglycerides (TG), Remnant Cholesterol (RC), Atherogenic Index (AI), Atherogenic Index of Plasma (AIP), Triglyceride Glucose Index (TyG), Lipoprotein Composite Index (LCI), Triglyceride to High-Density Lipoprotein Cholesterol Ratio (TG/HDL-C), Total Cholesterol to High-Density Lipoprotein Cholesterol Ratio (TC/HDL-C), Low-Density Lipoprotein Cholesterol to High-Density Lipoprotein Cholesterol Ratio (LDL-C/HDL-C), UHR) in the CKD group were significantly higher than those in the non-CKD group. The AUC analysis showed that HDL-C, AIP, TG/HDL-C, and UHR had strong predictive performance in the overall cohort and the non-CKD group, while in the CKD group, HDL-C, AI, and TC/HDL-C are better predictive indicators. After adjusting for all confounding factors, multivariate regression analysis revealed that HDL-C, apolipoprotein A-1 (APOA-1), and the APOA-1/APOB ratio were independent protective factors for CAD in the entire cohort. Among them, the protective effect of HDL-C was the most stable (overall population aOR = 0.26, 95% CI: 0.17–0.39, p < 0.001), and it was significantly in both the CKD (aOR = 0.18, 95% CI: 0.09–0.40, p < 0.001) and non-CKD subgroups (aOR = 0.31, 95% CI: 0.18–0.52, p < 0.001). In CKD, UHR is significantly correlated with CAD (aOR = 6.23, 95% CI: 1.89–20.60, p = 0.003), and the association was more significant in the non-CKD group (aOR = 15.15, 95% CI: 4.20–54.72, p < 0.001). CKD status significantly modified the association between UHR and CAD (P for interaction = 0.015). LOESS fitting suggested that UHR was positively correlated with the probability of CAD occurrence (the correlation was more significant at low UHR, and it slowed down when UHR > 0.5, r = 0.2, p < 0.001), and negatively correlated with eGFR (r = -0.38, p < 0.001). RCS analysis confirmed a significant nonlinear association between UHR and CAD (overall P < 0.001, nonlinear P = 0.002), and the risk of CAD increased when UHR was > 0.41 in CKD patients.

Conclusions

UHR is an independent risk factor for coronary heart disease, with higher adjusted OR values and more significant independent risk effects in non-CKD populations.