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TO THE EDITOR: We appreciate the great interest and comments provided on our paper [1]. We address Rigalleau and colleagues’ interest in the hypothesis of sarcopenia as a causal factor for chronic kidney disease (CKD) and the study limitations raised, including the use of estimated instead of measured glomerular filtration rates for the diagnosis of CKD and other issues. Sarcopenia has been considered to be a prevalent complication of CKD, especially for patients with more advanced stages of the disease, and etiologic factors of muscle derangements leading to muscle loss in CKD have been well documented. However, a reverse causation (in other words, sarcopenia as a risk factor for CKD) has not been fully evaluated. Several lines of evidence suggest that insulin resistance and its related adipokines play a pivotal role in kidney dysfunction [2]. Because skeletal muscle is integral to the development of insulin resistance, we can speculate that loss of muscle mass may lead to exacerbated insulin resistance, contributing to renal function decline. Moreover, our finding is in line with a recent longitudinal study by Fukuda et al., in which sarcopenic obesity was associated with rapid renal function decline in patients with type 2 diabetes [3]. We do acknowledge that future prospective trials are needed to better understand the natural course of CKD associated with longitudinal dynamic changes in body composition including skeletal muscle mass in patients with type 2 diabetes. As mentioned in our article, we used estimated glomerular function rate (eGFR) to assess the renal function, which may not be accurate in the setting of sarcopenia. However, the US Food and Drug Administration currently accepts eGFR decline as a surrogate end point for the development of kidney failure in clinical trials of kidney disease progression. Furthermore, we used the CKD Epidemiology Collaboration equation, which has been well validated and which is more accurate in Korean patients with type 2 diabetes and nephropathy [4]. Finally, the data on urine albumin excretion rates (AER) were not available in this study. As mentioned in our paper, we agree that it is a major limitation of our study as AER would have given further information on the effect of sarcopenia on kidney outcomes. As higher AER are associated with accelerated eGFR decline, there is a possibility that higher baseline AER found in the sarcopenic obesity group may have contributed to the different associations in sarcopenic only and sarcopenic obesity groups. However, a growing body of epidemiological evidence indicates that sarcopenia itself is also associated with increased risk of developing albuminuria in patients with diabetes [5]. Therefore, future studies assessing both AER and eGFR will be needed to verify this hypothesis. Nevertheless, our study has clearly demonstrated that sarcopenic obesity was independently associated with an increased risk of incident CKD in patients with type 2 diabetes.O