Sarcopenia or muscle wasting is a progressive and generalized skeletal muscle disorder involving the accelerated loss of muscle mass and function, often associated with muscle weakness (dynapenia) and frailty. Whereas primary sarcopenia is related to ageing, secondary sarcopenia happens independent of age in the context of chronic disease states such as chronic kidney disease (CKD). Sarcopenia has become a major focus of research and public policy debate due to its impact on patient's health-related quality of life, health-care expenditure, morbidity, and mortality. The development of sarcopenia in patients with CKD is multifactorial and it may occur independently of weight loss or cachexia including under obese sarcopenia. Hormonal imbalances can facilitate the development of sarcopenia in the general population and is a common finding in CKD. Hormones that may influence the development of sarcopenia are testosterone, growth hormone, insulin, thyroid hormones, and vitamin D. Although the relationship between free testosterone level that is low in uraemic patients and sarcopenia in CKD is not well-defined, functional improvement may be seen. Unlike testosterone, it is known that vitamin D is associated with muscle strength, muscle size, and physical performance in patients with CKD. Outcomes after vitamin D replacement therapy are still controversial. The half-life of growth hormone (GH) is prolonged in patients with CKD. Besides, IGF-1 levels are normal in patients with Stage 4 CKD—a minimal reduction is seen in the end-stage renal disease. Unresponsiveness or resistance of IGF-1 and changes in the GH/IGF-1 axis are the main causes of sarcopenia in CKD. Low serum T3 level is frequent in CKD, but the net effect on sarcopenia is not well-studied. CKD patients develop insulin resistance (IR) from the earliest period even before GFR decline begins. IR reduces glucose utilization as an energy source by hepatic gluconeogenesis, decreasing muscle glucose uptake, impairing intracellular glucose metabolism. This cascade results in muscle protein breakdown. IR and sarcopenia might also be a new pathway for targeting. Ghrelin, oestrogen, cortisol, and dehydroepiandrosterone may be other players in the setting of sarcopenia. In this review, we mainly examine the effects of hormonal changes on the occurrence of sarcopenia in patients with CKD via the available data.

中文翻译：

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激素变化对慢性肾病肌肉减少症的影响：我们现在在哪里，我们能做什么？

少肌症或肌肉萎缩是一种进行性和全身性骨骼肌疾病，涉及肌肉质量和功能的加速丧失，通常与肌肉无力（肌无力）和虚弱有关。原发性肌肉减少症与衰老有关，而继发性肌肉减少症的发生与慢性疾病状态（如慢性肾病 (CKD)）无关。肌肉减少症已成为研究和公共政策辩论的主要焦点，因为它对患者的健康相关生活质量、医疗保健支出、发病率和死亡率产生影响。CKD 患者发生肌肉减少症是多因素的，它可能与体重减轻或恶病质无关，包括肥胖的肌肉减少症。荷尔蒙失衡可促进一般人群中肌肉减少症的发展，并且是 CKD 的常见发现。可能影响肌肉减少症发展的激素是睾酮、生长激素、胰岛素、甲状腺激素和维生素 D。虽然尿毒症患者的游离睾酮水平低与 CKD 的肌肉减少症之间的关系尚不明确，但功能改善可能是见过。与睾酮不同，众所周知，维生素 D 与 CKD 患者的肌肉力量、肌肉大小和身体机能有关。维生素 D 替代疗法后的结果仍有争议。CKD 患者的生长激素 (GH) 半衰期延长。此外，4 期 CKD 患者的 IGF-1 水平是正常的——在终末期肾病患者中观察到最低限度的降低。IGF-1的无反应或抵抗以及GH/IGF-1轴的变化是CKD肌少症的主要原因。CKD 患者中血清 T3 水平较低很常见，但其对肌肉减少症的净影响尚未得到充分研究。CKD 患者甚至在 GFR 下降开始之前就开始出现胰岛素抵抗 (IR)。IR 通过肝糖异生降低作为能量来源的葡萄糖利用，减少肌肉葡萄糖摄取，损害细胞内葡萄糖代谢。这种级联反应导致肌肉蛋白质分解。IR 和肌肉减少症也可能是一种新的靶向途径。生长素释放肽、雌激素、皮质醇和脱氢表雄酮可能是导致肌肉减少症的其他因素。在这篇综述中，我们主要通过现有数据检查激素变化对 CKD 患者发生肌肉减少症的影响。CKD 患者甚至在 GFR 下降开始之前就开始出现胰岛素抵抗 (IR)。IR 通过肝糖异生降低作为能量来源的葡萄糖利用，减少肌肉葡萄糖摄取，损害细胞内葡萄糖代谢。这种级联反应导致肌肉蛋白质分解。IR 和肌肉减少症也可能是一种新的靶向途径。生长素释放肽、雌激素、皮质醇和脱氢表雄酮可能是导致肌肉减少症的其他因素。在这篇综述中，我们主要通过现有数据检查激素变化对 CKD 患者发生肌肉减少症的影响。CKD 患者甚至在 GFR 下降开始之前就开始出现胰岛素抵抗 (IR)。IR 通过肝糖异生降低作为能量来源的葡萄糖利用，减少肌肉葡萄糖摄取，损害细胞内葡萄糖代谢。这种级联反应导致肌肉蛋白质分解。IR 和肌肉减少症也可能是一种新的靶向途径。生长素释放肽、雌激素、皮质醇和脱氢表雄酮可能是导致肌肉减少症的其他因素。在这篇综述中，我们主要通过现有数据检查激素变化对 CKD 患者发生肌肉减少症的影响。IR 和肌肉减少症也可能是一种新的靶向途径。生长素释放肽、雌激素、皮质醇和脱氢表雄酮可能是导致肌肉减少症的其他因素。在这篇综述中，我们主要通过现有数据检查激素变化对 CKD 患者发生肌肉减少症的影响。IR 和肌肉减少症也可能是一种新的靶向途径。生长素释放肽、雌激素、皮质醇和脱氢表雄酮可能是导致肌肉减少症的其他因素。在这篇综述中，我们主要通过现有数据检查激素变化对 CKD 患者发生肌肉减少症的影响。