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Uraemic cardiomyopathy is characterized by myriad cardiac metabolic maladaptations, including altered mitochondrial function, changes in myocardial substrate utilization, altered metabolic transporter function and expression, and impaired insulin response and phosphoinositide-3 kinaseAKT signalling, which collectively lead to impaired cardiac energetics

Microbial metabolites also have an impact on bone metabolism

Sleep deprivation also increases cortisol levels, which promotes visceral fat deposition