Literature DB >> 30390262

Muscle Atrophy in Chronic Kidney Disease.

Jociane Schardong1, Miriam Allein Zago Marcolino2, Rodrigo Della Méa Plentz3,4,5.   

Abstract

The renal damage and loss of kidney function that characterize chronic kidney disease (CKD) cause several complex systemic alterations that affect muscular homeostasis, leading to loss of muscle mass and, ultimately, to muscle atrophy. CKD-induced muscle atrophy is highly prevalent and, in association with common CKD comorbidities, is responsible for the reduction of physical capacity, functional independence, and an increase in the number of hospitalizations and mortality rates. Thus, this chapter summarizes current knowledge about the complex interactions between CKD factors and the pathophysiological mechanisms that induce muscle atrophy that, despite growing interest, are not yet fully understood. The current treatments of CKD-induced muscle atrophy are multidisciplinary, including correction of metabolic acidosis, nutritional supplementation, reducing insulin resistance, administration of androgenic steroids, resisted and aerobic exercise, neuromuscular electrical stimulation, and inspiratory muscle training. However, further studies are still needed to strengthen the comprehension of CKD-induced muscle atrophy and the better treatment strategies.

Entities:  

Keywords:  Chronic kidney disease; Muscle atrophy; Pathophysiological mechanisms; Treatment

Mesh:

Year:  2018        PMID: 30390262     DOI: 10.1007/978-981-13-1435-3_18

Source DB:  PubMed          Journal:  Adv Exp Med Biol        ISSN: 0065-2598            Impact factor:   2.622


  7 in total

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4.  Calpain 6 inhibits autophagy in inflammatory environments: A preliminary study on myoblasts and a chronic kidney disease rat model.

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6.  Calycosin inhibited autophagy and oxidative stress in chronic kidney disease skeletal muscle atrophy by regulating AMPK/SKP2/CARM1 signalling pathway.

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Journal:  J Cachexia Sarcopenia Muscle       Date:  2021-11-01       Impact factor: 12.910

  7 in total

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