Atherosclerotic cardiovascular disease(AVD) is a major cause of the mortality and morbidity in end-stage renal disease(ESRD) patients undergoing chronic dialysis therapy. The factors such as lipopretein metabolism abnormality, diabetes, hypertension, hyperhomocysteinemia and oxidative stress have been implicated as underlying causes related AVD. Malnutrition, chronic inflammation, increased oxidative stress, hyperparathyroidism and its related lipoprotein abnormalities are suggested to accelerate AVD in ESRD patients. High-resolution B-mode ultrasono-graphy has been used to evaluate atherosclerotic change in carotid artery in a number of epidemiologic or clinical studies because of its non-invasive advantage and proven effects in predicting AVD or cardiovascular mortality. Using high-resolution B-mode sonography, we evaluated the presence of plaque and carotid intima-media area(cIM area), which is known to be a good predictor of athero-sclerosis. We compared and analyzed those sonographic findings according to a number of selected clinical and laboratory factors. Study subjects were 27 stable ESRD patient receiving hemodialysis(HD) or chronic ambulatory peritoneal dialysis(CAPD) at least over 24 months. The patients with present or past coronary, cerebral or peripheral vascular disease, history of anti-platelet agents or age over 70 years were excluded. Nine HD and 18 CAPD patients were included and mean age was 52.1+/-2.6 years and number of male and female patients were sixteen and eleven. Among many factors, sex, age, dialysis duration, diabetes, smoking history, blood pressure, body mass index, albumin, creatinine, high-density lipoprotein, triglyceride, C-reactive protein, total calcium, phosphorus, intact-parathyroidid hormone were selected and analyzed for their correlation with carotid sonograpic findings. 1) Mean cIM area of all patients was 15.4+/-0.7 mm2. cIM area was significantly increased in CAPD patients compared to HD patients(16.5+/-1.2 vs 14.9+/- 0.9mm2, p<0.05). Atherosclerotic plaques were found in 48.1% and bilateral lesion was found in 18.5% of all patients. The incidence of the plaque was 42.1% in HD and 55.6% in CAPD patients. 2) cIM area was more significantly increased in male than female(16.7+/-0.8 vs 13.6+/-1.2mm2, in diabetes than non-diabetes(16.4+/-0.8 vs 14.7+/-l.lmm2) and in smoker than non-smoker(18.8+/-0.7 vs 12.8+/-0.7mm2, p<0.05). It was also significantly inereased in patients with body mass index more than 2.3kg/ m(18.3+/-1.1 vs 14.6+/-0.8mm), systolic blood pres-sure more than 14mmHg(16.6+/-0.7 vs 13.0+/-1.2mm) and C-reactive pretein more than 0.5 mg/dL(18.9+/-1.5 vs 14.2+/-0.77mm2p<0.05). Among those factors, age, systolic blood pressure, body mass index and C-reactive protein were proven to positively correlate to cIM area with statistical significance(p<0.05). Even though cIM area was increased in patients with high serum parathyroid hormone, high total cholesterol and triglyceride and low high-density lipoprotein level, no statistical significances were found in these factors. 3) In comparison of each factor according to the presence of the plaque, age and the presence of diabetes were proven to be significantly different between patients without the plaque and with the plaque(45.7+/-2.7 vs 59.5+/-3.8 year, 33.3% vs 53.8%, respectively, p<0.05). Systolic blood pressure and C-reactive protein were increased in patients with the plaque but no statistical significance was shown. In conclusions, we found that old age, male sex, presence of diabetes, smoking history, high systolic blood pressure, increased body mass index and increased C-reactive protein were significantly related to increased cIM area and the plaque was more frequent in old age and diabetes patients using high resolution B-mode ultrasonography. It can be assumed that inflammatory state as reflected by C-reactive protein would be more related with atherosclerosis in ESRD patients than such as nutritional state, parathyroid hormone or lipoprotein metabolism based on these results. Fusing prospective analysis demonstrating causeeffect relationship or analyzing inflammatory index such as TNF-a or interleukin would be necessary to prove this assumption.