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Abstract：
Chronic kidney disease (CKD) is a progressive disorder associated with a decline in kidney function. Consequently, patients with advanced stages of CKD require renal replacement therapies, such as dialysis and kidney transplantation. Various conditions lead to the development of CKD, including diabetes mellitus, hypertension, and glomerulonephritis, among others. The disease is associated with metabolic and hormonal dysregulation, including uraemia and hyperparathyroidism, as well as with low-grade systemic inflammation. Altered homeostasis increases the risk of developing severe comorbidities, such as cardiovascular diseases or sarcopenia, which increase mortality. Sarcopenia is defined as a progressive decline in muscle mass and function. However, the precise mechanisms that link CKD and the development of sarcopenia are poorly understood. Knowledge about these linking mechanisms might lead to the introduction of precise treatment strategies that could prevent muscle wasting. This review discusses inflammatory mediators, metabolic and hormonal dysregulation, gut microbiota dysbiosis, and non-coding RNA alterations that could link CKD and sarcopenia.
摘要：
慢性肾病(CKD)是与肾功能下降相关的进行性疾病。因此,晚期CKD患者需要肾脏替代疗法，例如透析和肾移植。各种条件导致CKD的发展，包括糖尿病,高血压,肾小球肾炎,在其他人中。这种疾病与代谢和荷尔蒙失调有关，包括尿毒症和甲状旁腺功能亢进，以及低度全身性炎症。改变的体内平衡会增加发生严重合并症的风险，如心血管疾病或肌肉减少症，这增加了死亡率。肌肉减少症定义为肌肉质量和功能的进行性下降。然而,CKD与肌少症的发展之间的确切联系机制尚不清楚.对这些连接机制的了解可能会导致引入可以防止肌肉萎缩的精确治疗策略。这篇综述讨论了炎症介质，代谢和荷尔蒙失调，肠道菌群失调，以及可能连接CKD和肌少症的非编码RNA改变。
