scholarly journals Impaired skeletal muscle mitochondrial bioenergetics and physical performance in chronic kidney disease

JCI Insight ◽  
2020 ◽  
Vol 5 (5) ◽  
Author(s):  
Bryan Kestenbaum ◽  
Jorge Gamboa ◽  
Sophia Liu ◽  
Amir S. Ali ◽  
Eric Shankland ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Physical Performance ◽  
Mitochondrial Bioenergetics

scholarly journals Sarcopenia in chronic kidney disease – A brief review

2021 ◽  
Vol 35 (2) ◽  
Author(s):  
Beatriz Donato ◽  
◽  
Catarina Teixeira ◽  
Sónia Velho ◽  
Edgar Almeida ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Muscle Mass ◽  
Physical Performance ◽  
Functional Independence ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Dysfunction ◽  
Age Related ◽  
The Impact

Sarcopenia is a progressive age -related loss of muscle mass associated with a decline in muscle function and physical performance. Patients with chronic kidney disease experience substantial loss of muscle mass, weakness, and poor physical performance. Indeed, with the progression of chronic kidney disease, skeletal muscle dysfunction contributes to mobility limitation, loss of functional independence, and vulnerability to disease complications. There is a lack of robust data on the negative effect of the impact of kidney disease on skeletal muscle dysfunction, as well as on screening and treatment strategies that can be used in clinical practice to prevent functional decline and disability. Therefore, sarcopenia may be an underestimated condition with major implications for people with chronic kidney disease, even before the start of dialysis, which makes research into this topic necessary. The purpose of this review is to expand on some fundamental topics of sarcopenia, with an emphasis on the setting of chronic kidney disease patients.

Identification of the most clinically useful skeletal muscle mass indices pertinent to sarcopenia and physical performance in chronic kidney disease

Nephrology ◽  
2019 ◽  
Vol 25 (6) ◽  
pp. 467-474
Author(s):  
Thomas J. Wilkinson ◽  
Daniel G. D. Nixon ◽  
Danielle Richler‐Potts ◽  
Jill Neale ◽  
Yan Song ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Muscle Mass ◽  
Physical Performance ◽  
Skeletal Muscle Mass

Effect of Experimentally Induced Chronic Kidney disease on Skeletal, Cardiac and Smooth Muscle fibers of albino rat

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Ghada Lotfy ◽  
Amel Soliman ◽  
Nevine Bahaa ◽  
Mohammed Hegazi
Keyword(s):  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Smooth Muscle ◽  
Kidney Disease ◽  
Intramuscular Injection ◽  
Muscle Fibers ◽  
Lateral Wall ◽  
Control Group ◽  
Once Daily ◽  
Group Ii

Abstract Background Chronic kidney disease (CKD), or chronic renal failure (CRF) as it was historically termed, includes all degrees of decreased renal function, starting from mild, and moderate, to severe chronic kidney failure. Skeletal muscle atrophy frequently complicates the course of CKD and is associated with excess morbidity and mortality. Cardiovascular diseases have been reported to be the leading causes of death in CKD patients. Chronic Kidney Disease was also reported to be associated with an increased incidence of acid-related gastrointestinal disorders. Aim of the work The aim of this study was to investigate the effect of chronic kidney disease experimentally induced by gentamicin intramuscular injection on the histological structure of gastrocnemius skeletal muscle, left ventricular cardiac muscle and smooth muscle fibers of lower esophagus. Materials and methods Twenty male adult Wistar albino rats were randomly and equally divided into two groups. Group I (control group) received physiological saline intramuscular injection, once daily for 28 consecutive days, in a dose equivalent to that taken in group II. Group II (Gentamicin-treated group) were given Gentamicin intramuscular injection for induction of CKD. Gentamicin was given as Gentamycin sulfate, 40 mg/ml (Sandoz, Switzerland), once daily, in a dose of 80 mg/kg/day for 28 days to induce CKD. After 28 days of the first injection of gentamicin, rats were anaesthetized and blood samples were collected to measure the level of serum urea and creatinine. The left kidneys, the middle third of left gastrocnemius muscle, the lateral wall of left ventricle (LV) and the gastroesophageal junction of all rats of both groups (I and II) were processed for light microscopic study. The middle third of left gastrocnemius muscle, the lateral wall of left ventricle (LV) were further processed for transmission electron microscopic study. Histomorphometrical and statistical analysis were also done. Results The LM examination revealed moderate obliteration of glomeruli, dilatation in some renal tubules and collapse in others, mainly in distal convoluted tubules, with significant fibrosis of renal parenchyma. Serum urea and creatinine levels were increased significantly. The skeletal muscle fibers of the rats in group II (CKD) showed focal areas of myofibers degeneration with siginificant fibrosis. The cardiac muscle fibers of the rats in the group II (CKD) showed focal areas of cardiomyocytes degeneration and other areas of significantly hypertrophied fibers. The smooth muscle fibers of the lower esophageal sphincter of the rats in group II (CKD) showed no significant structural changes compared with the control group, however, the myenetric plexus showed multiple pyknotic and karyolitic nuclei with vacuolated cytoplasm. In addition, insignificant increase in the amount of collagen fibers was observed in almost all layers. Conclusion CKD produced moderate atrophy of skeletal muscle fibers, significant increase in the cardiomyocyte size and no significant structural effect of smooth muscle fibers of the lower esophageal sphincter.

scholarly journals Skeletal Muscle Regeneration and Oxidative Stress Are Altered in Chronic Kidney Disease

PLoS ONE ◽  
2016 ◽  
Vol 11 (8) ◽  
pp. e0159411 ◽  
Author(s):  
Keith G. Avin ◽  
Neal X. Chen ◽  
Jason M. Organ ◽  
Chad Zarse ◽  
Kalisha O’Neill ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration ◽  
And Oxidative Stress

scholarly journals Reductions in skeletal muscle mitochondrial mass are not restored following exercise training in patients with chronic kidney disease

2019 ◽  
Vol 34 (1) ◽  
pp. 1755-1767 ◽  
Author(s):  
Emma L. Watson ◽  
Luke A. Baker ◽  
Thomas J. Wilkinson ◽  
Douglas W. Gould ◽  
Matthew P.M. Graham‐Brown ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Exercise Training ◽  
Mitochondrial Mass

scholarly journals Atractylenolide III Attenuates Muscle Wasting in Chronic Kidney Disease via the Oxidative Stress-Mediated PI3K/AKT/mTOR Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Mingqing Wang ◽  
Rong Hu ◽  
Yanjing Wang ◽  
Lingyu Liu ◽  
Haiyan You ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Skeletal Muscles ◽  
Muscle Wasting ◽  
Mtor Pathway ◽  
C2c12 Myoblast ◽  
Model Group ◽  
Atractylenolide Iii

Oxidative stress contributes to muscle wasting in advanced chronic kidney disease (CKD) patients. Atractylenolide III (ATL-III), the major active constituent of Atractylodes rhizome, has been previously reported to function as an antioxidant. This study is aimed at investigating whether ATL-III has protective effects against CKD-induced muscle wasting by alleviating oxidative stress. The results showed that the levels of serum creatinine (SCr), blood urea nitrogen (BUN), and urinary protein significantly decreased in the ATL-III treatment group compared with the 5/6 nephrectomy (5/6 Nx) model group but were higher than those in the sham operation group. Skeletal muscle weight was increased, while inflammation was alleviated in the ATL-III administration group compared with the 5/6 Nx model group. ATL-III-treated rats also showed reduced dilation of the mitochondria, increased CAT, GSH-Px, and SOD activity, and decreased levels of MDA both in skeletal muscles and serum compared with 5/6 Nx model rats, suggesting that ATL-III alleviated mitochondrial damage and increased the activity of antioxidant enzymes, thus reducing the production of ROS. Furthermore, accumulated autophagosomes (APs) and autolysosomes (ALs) were reduced in the gastrocnemius (Gastroc) muscles of ATL-III-treated rats under transmission electron microscopy (TEM) together with the downregulation of LC3-II and upregulation of p62 according to Western blotting. This evidence indicated that ATL-III improved skeletal muscle atrophy and alleviated oxidative stress and autophagy in CKD rats. Furthermore, ATL-III could also increase the protein levels of p-PI3K, p-AKT, and p-mTOR in skeletal muscles in CKD rats. To further reveal the relevant mechanism, the oxidative stress-mediated PI3K/AKT/mTOR pathway was assessed, which showed that a reduced expression of p-PI3K, p-AKT, and p-mTOR in C2C12 myoblast atrophy induced by TNF-α could be upregulated by ATL-III; however, after the overexpression of Nox2 to increase ROS production, the attenuated effect was reversed. Our findings indicated that ATL-III is a potentially protective drug against muscle wasting via activation of the oxidative stress-mediated PI3K/AKT/mTOR pathway.

Quality over quantity? Association of skeletal muscle myosteatosis and myofibrosis on physical function in chronic kidney disease

2018 ◽  
Vol 34 (8) ◽  
pp. 1344-1353 ◽  
Author(s):  
Thomas J Wilkinson ◽  
Douglas W Gould ◽  
Daniel G D Nixon ◽  
Emma L Watson ◽  
Alice C Smith
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Physical Function ◽  
Physical Performance ◽  
Rating Scale ◽  
Handgrip Strength ◽  
Rectus Femoris ◽  
Muscle Quality ◽  
Muscle Size ◽  
Cross Sectional

Abstract Background Chronic kidney disease (CKD) is characterized by adverse changes in body composition, which are associated with poor clinical outcome and physical functioning. Whilst size is the key for muscle functioning, changes in muscle quality specifically increase in intramuscular fat infiltration (myosteatosis) and fibrosis (myofibrosis) may be important. We investigated the role of muscle quality and size on physical performance in non-dialysis CKD patients. Methods Ultrasound (US) images of the rectus femoris (RF) were obtained. Muscle quality was assessed using echo intensity (EI), and qualitatively using Heckmatt’s visual rating scale. Muscle size was obtained from RF cross-sectional area (RF-CSA). Physical function was measured by the sit-to-stand-60s (STS-60) test, incremental (ISWT) and endurance shuttle walk tests, lower limb and handgrip strength, exercise capacity (VO2peak) and gait speed. Results A total of 61 patients (58.5 ± 14.9 years, 46% female, estimated glomerular filtration rate 31.1 ± 20.2 mL/min/1.73 m2) were recruited. Lower EI (i.e. higher muscle quality) was significantly associated with better physical performance [STS-60 (r = 0.363) and ISWT (r = 0.320)], and greater VO2peak (r = 0.439). The qualitative rating was closely associated with EI values, and significant differences in function were seen between the ratings. RF-CSA was a better predictor of performance than muscle quality. Conclusions In CKD, increased US-derived EI was negatively correlated with physical performance; however, muscle size remains the largest predictor of physical function. Therefore, in addition to the loss of muscle size, muscle quality should be considered an important factor that may contribute to deficits in mobility and function in CKD. Interventions such as exercise could improve both of these factors.

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