Abstract:

Patients with chronic kidney disease (CKD) are often associated with different levels of protein-energy wasting (PEW) whose main clinical manifestation is skeletal muscle atrophy, which can increase the risk of complications and mortality. The pathogenesis of PEW is multifactorial. Previous studies suggested that loss of appetite, activation of the ubiquitin-proteasome system, and damage to the insulin/insulin-like growth factor l/phosphatidylinositol kinase/protein kinase B pathway were the main cause of muscle atrophy. With a lot of in-depth studies being finished in recent years, it has been found that inflammation, metabolic acidosis, hormone metabolism disorder, and myostatin expression increase also played important roles in the development and progress of muscle atrophy. At present, effective treatment for PEW is to add nutrients to ensure adequate intake of calories and protein. In addition, exercise, correction of metabolic acidosis, and improvement of inflammation in time also play roles in prevention and treatment of skeletal muscle atrophy in patients with CKD. Use of short-term hormone drugs can improve the body's protein storage, which lacks long-term researches on its efficacy and safety. It is still in the research stage to effectively block the catabolic pathways of skeletal muscle atrophy by targeting the ubiquitin proteasome system and myostatin signaling pathway, etc. A large number of experimental studies are still needed to explore effective measures for the prevention or treatment of PEW in patients with CKD.

Key words: Chronic kidney disease, Skeletal muscle atrophy, Pathogenesis, Treatment