Chronic kidney disease-induced muscle atrophy: Molecular mechanisms and promising therapies

Kexin Wang1, Qingyuan Liu2, Mingyu Tang3

  • 1Department of Nephrology, the Second Affiliated Hospital of Nantong University, Nantong, Jiangsu Province 226001, PR China; Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Jiangsu Clinical Medicine Center of Tissue Engineering and Nerve Injury Repair, Nantong University, Nantong, Jiangsu Province 226001, PR China.

Biochemical Pharmacology
|January 3, 2023
PubMed

Insights

Chronic kidney disease (CKD) causes muscle atrophy through inflammation and oxidative stress. Treatments targeting complications, nutrition, exercise, and drugs can improve patient outcomes.

Area of Science:

  • Nephrology
  • Muscle Physiology
  • Metabolic Disorders

Background:

  • Chronic kidney disease (CKD) is a significant health concern associated with high morbidity and mortality.
  • Muscle atrophy and sarcopenia are prevalent complications in CKD patients, severely impacting their quality of life.
  • The pathogenesis of muscle wasting in CKD is multifactorial, involving complex interactions between various mechanisms and contributing factors.

Purpose of the Study:

  • To comprehensively review the mechanisms underlying muscle atrophy in CKD.
  • To explore the roles of inflammation, oxidative stress, mitochondrial dysfunction, and other CKD-related complications in muscle wasting.
  • To identify and highlight potential therapeutic strategies for mitigating CKD-induced muscle atrophy.

Main Methods:

  • Literature review synthesizing current research on CKD-induced muscle atrophy.
  • Analysis of mechanisms including inflammation, oxidative stress, mitochondrial dysfunction, metabolic acidosis, vitamin D deficiency, anorexia, and angiotensin II excess.
  • Examination of contributing factors such as insulin resistance, hormonal changes, hemodialysis, uremic toxins, gut microbiota, and miRNA.

Main Results:

  • Inflammation, oxidative stress, and mitochondrial dysfunction are key drivers of muscle atrophy in CKD.
  • Metabolic acidosis, vitamin D deficiency, anorexia, and elevated angiotensin II exacerbate muscle wasting.
  • Insulin resistance, hormonal imbalances, hemodialysis, uremic toxins, gut dysbiosis, and altered miRNA profiles further contribute to sarcopenia in CKD.

Conclusions:

  • Understanding the multifaceted mechanisms of CKD-induced muscle atrophy is crucial for effective management.
  • Integrated treatment approaches, including complication management, nutritional support, physical activity, and pharmacological interventions, show promise.
  • Improving therapeutic strategies can enhance the prognosis and quality of life for CKD patients suffering from muscle atrophy.

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