Health-related fitness and quality of life following steroid withdrawal in renal transplant recipients

Painter, Patricia; Topp, Kimberly; Krasnoff, Joanne B.; Adey, Deborah; Strasner, Amy; Tomlanovich, S.; Stock, Philippe

doi:10.1046/j.1523-1755.2003.00038.x

Cited by 58 publications

(43 citation statements)

References 26 publications

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“…MS risk factors, such as glucose intolerance, itself an extremely common complication of renal transplantation (10) that contributes significantly to the cardiovascular risk factor profile of this patient group (11), are particularly important because they occur frequently in RTR (12). However, other factors that are relevant to renal transplantation, such as immunosuppression, renal dysfunction, and subclinical atherosclerosis, also may determine CF in RTR (13,14). To date, no studies have explored specifically the correlates of reduced CF in RTR.…”

mentioning

confidence: 99%

Cardiorespiratory Fitness Is Related to Physical Inactivity, Metabolic Risk Factors, and Atherosclerotic Burden in Glucose-Intolerant Renal Transplant Recipients

Armstrong¹,

Rakhit²,

Jeffriess³

et al. 2006

Clinical Journal of the American Society of Nephrology

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The mechanisms of reduced cardiorespiratory fitness (CF) in renal transplant recipients (RTR) have not been studied closely. This study evaluated the relationships between CF and specific cardiovascular risk factors (metabolic syndrome [MS], physical inactivity, myocardial ischemia, and atherosclerotic burden) in glucose-intolerant RTR. Data were recorded on 71 glucose-intolerant RTR (mean age 55 yr; 55% male; median transplant duration 5.7 yr). MS was defined using National Cholesterol Education Programme Adult Treatment Panel III criteria. Resting and exercise stress echocardiography were performed, and myocardial ischemia was identified by new or worsening wall motion abnormalities. Cardiorespiratory fitness was determined using peak oxygen uptake (VO 2 ) by expired gas analysis. Atherosclerotic burden was assessed by carotid intima-media thickness (IMT). Mean peak VO 2 was 19 ؎ 7 ml/kg per min and was significantly lower than predicted peak VO 2 (29 ؎ 6 ml/kg per min; P < 0.001). Patients with MS (63%) had reduced CF (17 ؎ 6 versus 22 ؎ 8 ml/kg per min; P ‫؍‬ 0.001) and were more likely to be physically inactive (76 versus 48%; P ‫؍‬ 0.02). CF was reduced in 14 patients with myocardial ischemia (15 ؎ 3 versus 20 ؎ 7 ml/kg per min; P ‫؍‬ 0.05). CF was positively correlated with male gender, height, and physical activity and inversely correlated with number of MS risk factors and IMT (adjusted R 2 ‫؍‬ 0.66). Carotid IMT added incremental value to clinical variables in determining VO 2 (adjusted R 2 ‫؍‬ 0.65 versus 0.63; P ‫؍‬ 0.04). Reduced CF is associated with physical inactivity, MS, and atherosclerotic burden in glucose-intolerant RTR. Further studies should address whether increasing exercise and modifying MS risk factors improve CF in RTR.

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mentioning

confidence: 99%

Cardiorespiratory Fitness Is Related to Physical Inactivity, Metabolic Risk Factors, and Atherosclerotic Burden in Glucose-Intolerant Renal Transplant Recipients

Armstrong¹,

Rakhit²,

Jeffriess³

et al. 2006

Clinical Journal of the American Society of Nephrology

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“…SKELETAL MUSCLE ATROPHY IS A COMMON FEATURE of several chronic diseases and is directly correlated with patient quality of life and mortality (30,31). Muscle atrophy results from an alteration of the balance between protein synthesis and degradation (19,34).…”

mentioning

confidence: 99%

REDD1 deletion prevents dexamethasone-induced skeletal muscle atrophy

Britto

Begue

Rossano

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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Ferry A, Bonnieu A, Ollendorff V, Favier FB. REDD1 deletion prevents dexamethasone-induced skeletal muscle atrophy. Am J Physiol Endocrinol Metab 307: E983-E993, 2014. First published October 14, 2014 doi:10.1152/ajpendo.00234.2014.-REDD1 (regulated in development and DNA damage response 1) has been proposed to inhibit the mechanistic target of rapamycin complex 1 (mTORC1) during in vitro hypoxia. REDD1 expression is low under basal conditions but is highly increased in response to several catabolic stresses, like hypoxia and glucocorticoids. However, REDD1 function seems to be tissue and stress dependent, and its role in skeletal muscle in vivo has been poorly characterized. Here, we investigated the effect of REDD1 deletion on skeletal muscle mass, protein synthesis, proteolysis, and mTORC1 signaling pathway under basal conditions and after glucocorticoid administration. Whereas skeletal muscle mass and typology were unchanged between wildtype (WT) and REDD1-null mice, oral gavage with dexamethasone (DEX) for 7 days reduced tibialis anterior and gastrocnemius muscle weights as well as tibialis anterior fiber size only in WT. Similarly, REDD1 deletion prevented the inhibition of protein synthesis and mTORC1 activity (assessed by S6, 4E-BP1, and ULK1 phosphorylation) observed in gastrocnemius muscle of WT mice following single DEX administration for 5 h. However, our results suggest that REDD1-mediated inhibition of mTORC1 in skeletal muscle is not related to the modulation of the binding between TSC2 and 14-3-3. In contrast, our data highlight a new mechanism involved in mTORC1 inhibition linking REDD1, Akt, and PRAS40. Altogether, these results demonstrated in vivo that REDD1 is required for glucocorticoidinduced inhibition of protein synthesis via mTORC1 downregulation. Inhibition of REDD1 may thus be a strategy to limit muscle loss in glucocorticoid-mediated atrophy. regulated in development and DNA damage response 1; protein synthesis; mechanistic target of rapamycin; autophagy; glucocorticoids; proline-rich Akt substrate of 40 kDa

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“…(12%), while the patients in the usual care group actually declined from 25.3 ± 6.5 to 23.7 ± 8.6 ml.kg −1 .min −1 (238). Although no significant differences were found between the two groups at the 3 month post-RTx baseline measures, the mean value in the steroid withdrawal group was 18% higher.…”

Section: Posttransplant Factors In Renal Transplantationmentioning

confidence: 53%

“…However, the steroid withdrawal study by Painter suggests that cardiovascular factors were not limiting. The role of corticosteroids in changes in exercise performance, body composition, and muscle strength was assessed through steroid withdrawal (238). Patients in the steroid withdrawal group improved theirVo 2peak during the 3 to 12 month post-RTx period from 21.5 to 24.1 ml.kg…”

Section: Posttransplant Factors In Renal Transplantationmentioning

confidence: 99%

Exercise Limitation Following Transplantation

Williams

McKenna

2012

Comprehensive Physiology

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Organ transplantation is one of the medical miracles or the 20th century. It has the capacity to substantially improve exercise performance and quality of life in patients who are severely limited with chronic organ failure. We focus on the most commonly performed solid‐organ transplants and describe peak exercise performance following recovery from transplantation. Across all of the common transplants, evaluated significant reduction in o 2 peak is seen (typically renal and liver 65%‐80% with heart and/or lung 50%‐60% of predicted). Those with the lowest o 2 peak pretransplant have the lowest o 2 peak posttransplant. Overall very few patients have a o 2 peak in the normal range. Investigation of the cause of the reduction of o 2 peak has identified many factors pre‐ and posttransplant that may contribute. These include organ‐specific factors in the otherwise well‐functioning allograft (e.g., chronotropic incompetence in heart transplantation) as well as allograft dysfunction itself (e.g., chronic lung allograft dysfunction). However, looking across all transplants, a pattern emerges. A low muscle mass with qualitative change in large exercising skeletal muscle groups is seen pretransplant. Many factor posttransplant aggravate these changes or prevent them recovering, especially calcineurin antagonist drugs which are key immunosuppressing agents. This results in the reduction of o 2 peak despite restoration of near normal function of the initially failing organ system. As such organ transplantation has provided an experiment of nature that has focused our attention on an important confounder of chronic organ failure‐skeletal muscle dysfunction. © 2012 American Physiological Society. Compr Physiol 2:1937‐1979, 2012.

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Health-related fitness and quality of life following steroid withdrawal in renal transplant recipients

Cited by 58 publications

References 26 publications

Cardiorespiratory Fitness Is Related to Physical Inactivity, Metabolic Risk Factors, and Atherosclerotic Burden in Glucose-Intolerant Renal Transplant Recipients

Cardiorespiratory Fitness Is Related to Physical Inactivity, Metabolic Risk Factors, and Atherosclerotic Burden in Glucose-Intolerant Renal Transplant Recipients

REDD1 deletion prevents dexamethasone-induced skeletal muscle atrophy

Exercise Limitation Following Transplantation

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