Muscle wasting and energy balance in critical illness

Reid, Clare; Campbell, Iain; Little, R. A.

doi:10.1016/s0261-5614(03)00129-8

Cited by 216 publications

(183 citation statements)

References 21 publications

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“…However, large improvements in GFR from baseline after critical illness would seem implausible, whereas large and sustained falls in creatinine generation have been shown in animal models of sepsis (14), patients with advanced CKD (15), and critically ill humans (16)(17)(18), with greatest decrease occurring in the sickest patients (16). Skeletal muscle is the major source of creatinine production, and critical illness is associated with profound loss of skeletal muscle protein (10,19,20), with muscle thickness steadily decreasing over time after ICU admission (10,21,22). Loss of muscle mass can persist long after hospital discharge (23).…”

Section: Study Findingsmentioning

confidence: 99%

Serum Creatinine Changes Associated with Critical Illness and Detection of Persistent Renal Dysfunction after AKI

Prowle

Kolic²,

Purdell-Lewis³

et al. 2014

Clinical Journal of the American Society of Nephrology

141

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Background and objectives AKI is a risk factor for development or worsening of CKD. However, diagnosis of renal dysfunction by serum creatinine could be confounded by loss of muscle mass and creatinine generation after critical illness.Design, setting, participants, & measurements A retrospective, single center analysis of serum in patients surviving to hospital discharge with an intensive care unit admission of 5 or more days between 2009 and 2011 was performed.Results In total, 700 cases were identified, with a 66% incidence of AKI. In 241 patients without AKI, creatinine was significantly lower (P,0.001) at hospital discharge than admission (median, 0.61 versus 0.88 mg/dl; median decrease, 33%). In 160 patients with known baseline, discharge creatinine was significantly lower than baseline in all patients except those patients with severe AKI (Kidney Disease Improving Global Outcomes category 3), who had no significant difference. In a multivariable regression model, median duration of hospitalization was associated with a predicted 30% decrease (95% confidence interval, 8% to 45%) in creatinine from baseline in the absence of AKI; after allowing for this effect, AKI was associated with a 29% (95% confidence interval, 10% to 51%) increase in predicted hospital discharge creatinine. Using a similar model to exclude the confounding effect of prolonged major illness on creatinine, 148 of 700 patients (95% confidence interval, 143 to 161) would have eGFR,60 ml/min per 1.73 m 2 at hospital discharge compared with only 63 of 700 patients using eGFR based on unadjusted hospital creatinine (a 135% increase in potential CKD diagnoses; P,0.001).Conclusion Critical illness is associated with significant falls in serum creatinine that persist to hospital discharge, potentially causing inaccurate assessment of renal function at discharge, particularly in survivors of AKI. Prospective measurements of GFR and creatinine generation are required to confirm the significance of these findings.

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Section: Study Findingsmentioning

confidence: 99%

Serum Creatinine Changes Associated with Critical Illness and Detection of Persistent Renal Dysfunction after AKI

Prowle

Kolic²,

Purdell-Lewis³

et al. 2014

Clinical Journal of the American Society of Nephrology

141

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“…In C 2 C 12 skeletal myotubes incubated with TNF-a for a 48-hour period, however, the opposite effect had been observed (i.e., TNF-a markedly depressed electrically evoked Ca 21 transients [42]). It is very likely that some of the multiple suggested slow signaling mechanisms involved in cytokinemediated muscle weakness (reactive oxygen species, nitric oxide production, peroxidation, ATP depletion [5]) respond differentially to different prolonged exposure time versus concentration products. However, in the case of IL-1a in our study, it is highly unlikely that second messenger-related pathways contributed significantly to the observed effects in our skinned fiber preparation, where the myoplasmic environment is in equilibrium with a defined indefinite bath volume controlling the fiber cytosol, and no longer containing signaling molecules in any significant amounts (calculated dilution .1:10 6 ).…”

Section: Concentration Effects Of Il-1 and Potential Relations To Sepmentioning

confidence: 99%

IL-1α Reversibly Inhibits Skeletal Muscle Ryanodine Receptor. A Novel Mechanism for Critical Illness Myopathy?

Friedrich

Edwards

et al. 2014

Am J Respir Cell Mol Biol

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Critical illness myopathies in patients with sepsis or sustained mechanical ventilation prolong intensive care treatment and threaten both patients and health budgets; no specific therapy is available. Underlying pathophysiological mechanisms are still patchy. We characterized IL-1a action on muscle performance in "skinned" muscle fibers using force transducers and confocal Ca (1) increased SR Ca 21 retention, (2) increased IL-1a force transients being reproduced by 25 mM tetracaine, and (3) reduced Ca 21 spark frequencies by IL-1a or tetracaine. Coimmunoprecipitation confirmed RyR1/IL-1 association. RyR1/IL-1 immunofluorescence patterns perfectly colocalized. Long-term, 8-hour IL-1a challenge of intact muscle fibers compromised membrane integrity in approximately 50% of fibers, and confirmed intracellular IL-1a deposition. IL-1a exerts a novel, specific, and reversible interaction mechanism with the skeletal muscle RyR1 macromolecular release complex without the need to act via its membrane IL-1 receptor, as IL-1R membrane expression levels were not detectable in Western blots or immunostaining of single fibers. We present a potential explanation of how the inflammatory mediator, IL-1a, may contribute to muscle weakness in critical illness.

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“…Patients with fibrotic lung disease can develop acute respiratory failure due to an exacerbation of their underlying disease. These acute exacerbations are characterized pathologically by diffuse alveolar damage (3), which is also the most common pathologic finding in acute respiratory distress syndrome (ARDS) (4,5). Given the radiologic and pathologic similarities between exacerbations of fibrotic lung disease and ARDS, and to further explore the increased risk of death from respiratory failure associated with interstitial lung abnormalities, we sought to determine whether interstitial lung abnormalities on prior CT imaging were associated with an increased risk of ARDS, in a cohort of patients with sepsis or the systemic inflammatory response syndrome (SIRS).…”

Section: Interstitial Lung Abnormalities Are Associated With Acute Rementioning

confidence: 99%

Rectus Femoris Cross-Sectional Area and Muscle Layer Thickness: Comparative Markers of Muscle Wasting and Weakness

Puthucheary

McNelly

Rawal

et al. 2017

Am J Respir Crit Care Med

109

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Muscle wasting and energy balance in critical illness

Cited by 216 publications

References 21 publications

Serum Creatinine Changes Associated with Critical Illness and Detection of Persistent Renal Dysfunction after AKI

Serum Creatinine Changes Associated with Critical Illness and Detection of Persistent Renal Dysfunction after AKI

IL-1α Reversibly Inhibits Skeletal Muscle Ryanodine Receptor. A Novel Mechanism for Critical Illness Myopathy?

Rectus Femoris Cross-Sectional Area and Muscle Layer Thickness: Comparative Markers of Muscle Wasting and Weakness

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