Pathogenesis of Sarcopenia in Chronic Kidney Disease-The Role of Inflammation, Metabolic Dysregulation, Gut Dysbiosis, and microRNA.
Estera BakinowskaJoanna Olejnik-WojciechowskaKajetan KiełbowskiAnastasiia SkorykAndrzej PawlikPublished in: International journal of molecular sciences (2024)
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.
Keyphrases
- chronic kidney disease
- end stage renal disease
- skeletal muscle
- low grade
- kidney transplantation
- community dwelling
- oxidative stress
- cardiovascular disease
- multiple sclerosis
- high grade
- healthcare
- blood pressure
- insulin resistance
- cardiovascular events
- early onset
- drug induced
- peritoneal dialysis
- adipose tissue
- arterial hypertension