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    Epicardial Adipose Tissue and Coronary Artery Calcification in Diabetic and Nondiabetic End-Stage Renal Disease Patients
    (TAYLOR & FRANCIS LTD, 2011) Tonbul, Halil Zeki; Turkmen, Kultigin; Kayikcioglu, Hatice; Ozbek, Orhan; Kayrak, Mehmet; Biyik, Zeynep
    Background/aims: Atherosclerosis, coronary artery calcification, diabetes mellitus, inflammation, endothelial dysfunction, and left ventricular hypertrophy are the most commonly encountered risk factors in the pathogenesis of cardiovascular disease in end-stage renal disease (ESRD) patients. Epicardial adipose tissue (EAT) is the true visceral fat depot of the heart. The relationship between coronary artery disease (CAD) and EAT was shown in healthy subjects and patients with high risk of CAD. To date, there is not enough data about EAT in diabetic and nondiabetic ESRD patients. Therefore, we aimed to investigate the EAT and coronary artery calcification score (CACS) in diabetic and nondiabetic ESRD patients and healthy subjects. Methods: Sixty ESRD patients (17 diabetic, 43 nondiabetic ESRD patients) and 20 healthy subjects were enrolled in the study. EAT and CACS were performed by a 64-slice multidetector computed tomography scanner. Results: There were no differences in age, gender, body mass index, pre-dialysis systolic and diastolic blood pressure levels, biochemical parameters including serum low-density lipoprotein and high-density lipoprotein cholesterol, triglycerides, and C-reactive protein between healthy subjects, diabetic, and nondiabetic ESRD patients. Total CACSs and EAT measurements were significantly higher in diabetic ESRD patients when compared with nondiabetic ESRD patients and healthy subjects. There was statistically significant relationship between EAT and CACS in ESRD patients (p < 0.0001, r = 0.48). Conclusion: In conclusion, we found a significant increase in terms of EAT and CACS in diabetic ESRD patients when compared with nondiabetic ESRD patients and healthy subjects.
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    The Relationship between Epicardial Adipose Tissue and Malnutrition, Inflammation, Atherosclerosis/Calcification Syndrome in ESRD Patients
    (AMER SOC NEPHROLOGY, 2011) Turkmen, Kultigin; Kayikcioglu, Hatice; Ozbek, Orhan; Solak, Yalcin; Kayrak, Mehmet; Samur, Cigdem; Anil, Melih
    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