Ji Cheol Bae1, Ji Min Han1, Sam Kwon1, Jae Hwan Jee2, Tae Yang Yu3, Moon Kyu Lee3, Jae Hyeon Kim4. 1. Division of Endocrinology and Metabolism, Department of Medicine, Samsung Changwon Hospital, Sungkyunkwan University School of Medicine, Changwon, 630-723, Republic of Korea. 2. Department of Health Promotion Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, 135-710, Republic of Korea. 3. Division of Endocrinology and Metabolism, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, 135-710, Republic of Korea. 4. Division of Endocrinology and Metabolism, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, 135-710, Republic of Korea; Department of Clinical Research Design and Evaluation, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul, 135-710, Republic of Korea. Electronic address: jaehyeon@skku.edu.
Abstract
BACKGROUND AND AIMS: The objective of this study was to evaluate the ability of lipid variables to predict the development of chronic kidney disease (CKD). We investigated the longitudinal association between lipid profiles and incident CKD in a large apparently healthy cohort. METHODS: A retrospective longitudinal analysis of 10,288 subjects who had participated in comprehensive health check-ups at least four times over a 7-year period was conducted. The risk of incident CKD associated with lipid variables was analyzed using adjusted hazard ratio (HR) for CKD per 1 standard deviation (SD) increase in lipid level. The development of CKD was defined as estimated glomerular filtration rate <60 ml/min/1.73 m(2). RESULTS: Over a mean follow-up of 56.5 ± 14.3 months, 356 (3.5%) subjects developed CKD. The multivariate adjusted HRs for incident CKD per 1 SD increase in baseline lipid level were 1.29 (95% confidence interval [CI], 1.17-1.41) for triglycerides (TG), 0.77 (0.68-0.88) for high-density lipoprotein cholesterol (HDL-C), 1.22 (1.12-1.32) for the TG/HDL-C ratio, 0.82 (0.73-0.92) for the low-density lipoprotein cholesterol/apolipoprotein B (LDL-C/apoB) ratio, and 0.74 (0.66-0.83) for the HDL-C/apoA-1 ratio. No longitudinal association was found between incident CKD and baseline total cholesterol, LDL-C, non-HDL-C, the LDL-C/HDL-C ratio, apoB, apoA-I, or the apoB/apoA-I ratio. CONCLUSIONS: The LDL-C/apoB and HDL-C/apoA-1 ratios as well as TG and HDL-C concentrations independently predicted an increased risk for developing CKD. Our findings suggest that particle size of HDLs and LDLs may contribute to the development of CKD.
BACKGROUND AND AIMS: The objective of this study was to evaluate the ability of lipid variables to predict the development of chronic kidney disease (CKD). We investigated the longitudinal association between lipid profiles and incident CKD in a large apparently healthy cohort. METHODS: A retrospective longitudinal analysis of 10,288 subjects who had participated in comprehensive health check-ups at least four times over a 7-year period was conducted. The risk of incident CKD associated with lipid variables was analyzed using adjusted hazard ratio (HR) for CKD per 1 standard deviation (SD) increase in lipid level. The development of CKD was defined as estimated glomerular filtration rate <60 ml/min/1.73 m(2). RESULTS: Over a mean follow-up of 56.5 ± 14.3 months, 356 (3.5%) subjects developed CKD. The multivariate adjusted HRs for incident CKD per 1 SD increase in baseline lipid level were 1.29 (95% confidence interval [CI], 1.17-1.41) for triglycerides (TG), 0.77 (0.68-0.88) for high-density lipoprotein cholesterol (HDL-C), 1.22 (1.12-1.32) for the TG/HDL-C ratio, 0.82 (0.73-0.92) for the low-density lipoprotein cholesterol/apolipoprotein B (LDL-C/apoB) ratio, and 0.74 (0.66-0.83) for the HDL-C/apoA-1 ratio. No longitudinal association was found between incident CKD and baseline total cholesterol, LDL-C, non-HDL-C, the LDL-C/HDL-C ratio, apoB, apoA-I, or the apoB/apoA-I ratio. CONCLUSIONS: The LDL-C/apoB and HDL-C/apoA-1 ratios as well as TG and HDL-C concentrations independently predicted an increased risk for developing CKD. Our findings suggest that particle size of HDLs and LDLs may contribute to the development of CKD.