Study purpose Evidence on the effects of sarcopenic obesity (SO) on incident chronic kidney disease (CKD) and rapid kidney function decline (RKFD) in the Chinese population is limited. This study aimed to prospectively examine the associations of SO with incident CKD and RKFD among middle-aged and older Chinese adults.Study design and methods This prospective cohort study utilized data from the China Health and Retirement Longitudinal Study (CHARLS), a nationally representative longitudinal study of Chinese adults aged 45 and older. The analysis included 4201 individuals from the 2011 wave, with renal outcomes ascertained from the 2015 wave. The effects of SO on incident CKD and RKFD were assessed using logistic regression models. Robustness was tested through subgroup and sensitivity analyses.Results Over four years of follow-up, 228 cases of incident CKD and 213 cases of RKFD were observed. After multivariable adjustment, participants in the "sarcopenic obesity" group showed a 78% increased risk of incident CKD (odds ratio [OR] 1.78, 95% confidence interval [CI] 1.09-2.90) and a 79% increased risk of RKFD (OR 1.79, 95% CI 1.03-3.13), compared to the "nonsarcopenia without obesity" group. Consistent results were observed across subgroups stratified by gender, education level, marital status, geographic area, lifestyle factors, and comorbidities, with no significant interactions detected.Conclusions In a population-based cohort of middle-aged and older Chinese adults, SO was independently associated with elevated risks of incident CKD and RKFD, without interaction effects. These findings underscore the importance of timely intervention for SO to prevent adverse kidney outcomes. Key message What is already known on this topic? The relationship between sarcopenic obesity (SO) and the risk of chronic kidney disease (CKD) and renal function decline has been established in Korean and Japanese individuals with type 2 diabetes mellitus. However, it is uncertain if these findings apply to other populations, particularly those without diabetes. Additionally, the influence of diabetes on these associations needs further exploration, and the link between SO and rapid kidney function decline (RKFD) remains unestablished. Evidence regarding the effects of SO on incident CKD and RKFD in the Chinese population is limited, highlighting the necessity for this study to fill these gaps in knowledge. What this study adds This study is the first to prospectively explore the association of SO with incident CKD and RKFD in middle-aged and older Chinese adults. We identified SO as a significant risk factor for increased incidence of both CKD and RKFD. These findings expand the understanding of the impact of SO beyond individuals with diabetes mellitus, indicating that SO is a universal risk factor for adverse kidney outcomes in aging populations, irrespective of demographic and health characteristics. How this study might affect research, practice, or policy This study identifies SO as an independent risk factor for incident CKD and RKFD in middle-aged and older Chinese adults. The findings suggest that SO is a modifiable risk factor for kidney health, underscoring the necessity for timely interventions to prevent adverse kidney outcomes. Given the rising prevalence of SO and kidney disease in aging populations worldwide, these results highlight the importance of incorporating SO management into public health and clinical strategies. Questions pending answer What role do specific lifestyle factors (e.g. diet, physical activity) play in mitigating or exacerbating kidney function decline in individuals with SO? Are there genetic markers that predispose individuals with SO to a higher risk of incident CKD and RKFD? What are the underlying molecular mechanisms linking SO to incident CKD and RKFD?Conclusions In a population-based cohort of middle-aged and older Chinese adults, SO was independently associated with elevated risks of incident CKD and RKFD, without interaction effects. These findings underscore the importance of timely intervention for SO to prevent adverse kidney outcomes. Key message What is already known on this topic? The relationship between sarcopenic obesity (SO) and the risk of chronic kidney disease (CKD) and renal function decline has been established in Korean and Japanese individuals with type 2 diabetes mellitus. However, it is uncertain if these findings apply to other populations, particularly those without diabetes. Additionally, the influence of diabetes on these associations needs further exploration, and the link between SO and rapid kidney function decline (RKFD) remains unestablished. Evidence regarding the effects of SO on incident CKD and RKFD in the Chinese population is limited, highlighting the necessity for this study to fill these gaps in knowledge. What this study adds This study is the first to prospectively explore the association of SO with incident CKD and RKFD in middle-aged and older Chinese adults. We identified SO as a significant risk factor for increased incidence of both CKD and RKFD. These findings expand the understanding of the impact of SO beyond individuals with diabetes mellitus, indicating that SO is a universal risk factor for adverse kidney outcomes in aging populations, irrespective of demographic and health characteristics. How this study might affect research, practice, or policy This study identifies SO as an independent risk factor for incident CKD and RKFD in middle-aged and older Chinese adults. The findings suggest that SO is a modifiable risk factor for kidney health, underscoring the necessity for timely interventions to prevent adverse kidney outcomes. Given the rising prevalence of SO and kidney disease in aging populations worldwide, these results highlight the importance of incorporating SO management into public health and clinical strategies. Questions pending answer What role do specific lifestyle factors (e.g. diet, physical activity) play in mitigating or exacerbating kidney function decline in individuals with SO? Are there genetic markers that predispose individuals with SO to a higher risk of incident CKD and RKFD? What are the underlying molecular mechanisms linking SO to incident CKD and RKFD?
