4.6 Article

The Relationship between Epicardial Adipose Tissue and Malnutrition, Inflammation, Atherosclerosis/Calcification Syndrome in ESRD Patients

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AMER SOC NEPHROLOGY
DOI: 10.2215/CJN.00890111

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  1. Scientific Investigation and Project Foundation of Selcuk University Meram School of Medicine

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Background and objectives Malnutrition, inflammation, atherosclerosis/calcification (MIAC) and endothelial dysfunction are the most commonly encountered risk factors in the pathogenesis of cardiovascular disease in ESRD patients. Epicardial adipose tissue (EAT) is the true visceral fat depot of the heart. The relationship between CAD and EAT was shown in patients with high risk of coronary artery disease. In this study, we aimed to investigate the relationship between EAT and MIAC syndrome in ESRD patients. Design, setting, participants, & measurements Eighty ESRD patients and 27 healthy subjects enrolled in this cross-sectional study. EAT and coronary artery calcification score were measured by a multidetector computed tomography (MDCT) scanner. Patients with serum albumin <3.5 mg/dl were defined as patients with malnutrition; those with serum C-reactive protein level >10 ng/dl (normal range, 0-5 ng/dl) had inflammation; and those with CACS >10 had atheroscleosis/calcification. Results Total CACS and EAT measurements were significantly higher in ESRD patients when compared with healthy subjects. There was a statistically significant relationship between EAT and CACS in ESRD patients (r = 0.48). EAT measurements were higher in PD patients than HD patients. Twenty-four of the patients had no component, 31 had one component, 17 had two components, and nine had all of the MIAC components. EAT was found to be significantly increased when the presence of MIAC components increased. EAT was positively correlated with age, body mass index, and presence of MIAC. These parameters were also found as independent predictors of increased EAT. Conclusions We found a relationship between EAT and components of MTAC syndrome in ESRD patients. J Am Soc Nephrol 6: 1920-1925, 2011. doi: 10.2215/CJN.00890111

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