The Role of Remnant Cholesterol and Its Interaction with Low-Density Lipoprotein Cholesterol in Chronic Kidney Disease

Abstract

Background The growing prevalence of chronic kidney disease (CKD) presents a substantial public health issue. Furthermore, the continuous advancements in lipid-lowering strategies and medications highlight the ongoing importance of the correlation between remnant cholesterol (RC) and CKD. This study aims to investigate the link between RC and CKD risk, particularly focusing on the interplay between low-density lipoprotein cholesterol (LDL-C) and RC. Methods This cross-sectional study included 7747 participants in wave 2009 of the China Health and Nutrition Survey which has been in progress since 1989. We enrolled 7747 individuals in the present study from the China Health and Nutrition Survey, with exclusion criteria applied to individuals under 18 and pregnant participants. CKD was defined as eGFR < 60 mL/min/1.73 m², following the Kidney Disease: Improving Global Outcomes (KDIGO) 2012 Clinical Practice Guideline. A logistic regression analysis was conducted to assess the associations between discordant/concordant levels of LDL-C and RC with CKD. Subsequently, a mediation analysis was performed to identify potential mediators. Results Within the clinical cohort of 7747 patients, 910 individuals (11.8%) were diagnosed with CKD, with RC levels categorized into quartiles. Logistic analysis revealed significant associations between elevated RC levels and the prevalence of CKD (OR 1.30, 95% CI 1.06–1.60 for Group 2; OR 1.49, 95% CI 1.22–1.83 for Group 3; and OR 1.33, 95% CI 1.08–1.63 for Group 4). The results of restricted cubic splines (RCS) analysis suggested an “inverted U-shaped” association of RC with CKD. The analysis of discordant/concordant grouping showed that participants in Group 2 (high LDL-C/low RC) and Group 3 (low LDL-C/high RC) were associated with an increased risk for CKD. The odds ratios were 2.35 (95% CI 1.83–3.03) for Group 2 and 1.51 (95% CI 1.14–2.01) for Group 3, compared to Group 1 (low LDL-C/low RC). Causal mediation analysis indicated that inflammation partially mediated the association between RC and CKD. Conclusions This study presented evidence of a non-linear relationship between RC and CKD, suggesting that the association was influenced by LDL-C levels and mediated by the pro-inflammatory state.