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Abstract: TH-PO828

Molecular Mechanisms Underpinning Muscle Atrophy in CKD

Session Information

Category: Health Maintenance‚ Nutrition‚ and Metabolism

  • 1400 Health Maintenance‚ Nutrition‚ and Metabolism


  • Wong, Limy, Monash University Eastern Health Clinical School, Box Hill, Victoria, Australia
  • Kenny, Rachel, Monash University Eastern Health Clinical School, Box Hill, Victoria, Australia
  • Howard, Jennifer L., Eastern Health Foundation, Box Hill, Victoria, Australia
  • McMahon, Lawrence P., Monash University Eastern Health Clinical School, Box Hill, Victoria, Australia

Sarcopenia is prevalent in patients with chronic kidney disease (CKD). Emerging evidence reports the association of sarcopenia with poor outcomes. The underlying molecular pathogenesis has yet to be fully elucidated. The aim of this systematic review is to summarise the current evidence on molecular mechanisms underpinning muscle atrophy in CKD and to assess the strength of such evidence.


The PubMed and EMBASE databases were searched using 3 main themes: mRNA/protein/microRNA expression, skeletal muscle and CKD. This study was conducted in accordance with the PRISMA standards (Figure 1) and was registered with PROSPERO (CRD42021257292).


Ninety-eight studies were included in the systematic review, comprising 26 prospective human clinical studies, 4 human and rodent studies, and 68 rodent-only studies (32 mouse and 36 rat models respectively). The sample sizes of human studies were predominantly small (40% of studies had ≤20 participants). Qualitative polymerase chain reaction (qPCR) was the most commonly used method for gene expression. None of the studies fulfilled the Minimum Information for Publication of qPCR Experiments (MIQE) criteria for quality assessment. Most studies investigated only a few genes or a specific signalling pathway. FBXO32, TRIM63, MSTN, IL6, TNF and IGF1 were the most studied genes. The identified differentially expressed genes and proteins belonged to 8 major pathways, including apoptosis, autophagy, inflammation, insulin/insulin-like growth factor 1 signalling, lipid metabolism, mitochondrial function, muscle cell growth and differentiation, and protein degradation, similar to other chronic disease states.


The current evidence for molecular mechanisms of muscle atrophy in CKD is largely derived from small and heterogeneous studies. Nonetheless, comparable modifications in the major biological pathways between CKD and other chronic diseases supports shared deleterious molecular mechanisms producing muscle atrophy, irrespective of the underlying chronic disease.


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