Sarcopenia in Chronic Kidney Disease: Focus on Advanced Glycation End Products as Mediators and Markers of Oxidative Stress

Sarcopenia is common in chronic kidney disease (CKD), and it is independently associated with morbidity and mortality. Advanced glycation end products (AGE) are mainly known as aging products. In CKD, AGE accumulate due to increased production and reduced kidney excretion. The imbalance between oxidant/antioxidant capacities in CKD patients is one of the main factors leading to AGE synthesis. AGE can, in turn, promote CKD progression and CKD-related complications by increasing reactive oxygen species generation, inducing inflammation, and promoting fibrosis. All these derangements can further increase AGE and uremic toxin accumulation and promote loss of muscle mass and function. Since the link between AGE and sarcopenia in CKD is far from being fully understood, we revised hereby the data supporting the potential contribution of AGE as mediators of oxidative stress in the pathogenesis of sarcopenia. Understanding how AGE and oxidative stress impact the onset of sarcopenia in CKD may help to identify new potential markers of disease progression and/or therapeutic targets.

Automated summary

Sarcopenia in chronic kidney disease is independently associated with morbidity and mortality, with advanced glycation end products (AGE) playing a key role in its pathogenesis. The imbalance of oxidant/antioxidant capacities in CKD patients leads to AGE accumulation, which can promote CKD progression and related complications by inducing inflammation and fibrosis. Understanding the link between AGE and oxidative stress in the onset of sarcopenia may help identify new markers for disease progression and therapeutic targets.