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      Ultrasonic Tissue Characterization of the Carotid Artery in Chronic Renal Failure Patients

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          The ultrasonic reflectivity of the carotid wall, measured by means of integrated backscatter (IBS) analysis, has recently been evaluated in patients with atherosclerotic diseases and it was considered to be a prognostic marker. We performed B-mode measurement and IBS analysis of the carotid wall in 30 chronic renal failure (CRF) patients (serum creatinine 548 ± 230 µmol/l) on conservative treatment and free of clinical evidence of cardiovascular complications; 14 were normotensives (NT) and 16 were treated hypertensives (TH). Thirty sex- and age-matched healthy subjects served as controls. The IBS carotid index was significantly higher in CRF patients than in controls (31.7 ± 3.5 vs. 28.9 ± 2.3 dB; p < 0.001), and no difference was observed between TH and NT CRF patients. The IBS index was negatively correlated with low-density lipoprotein cholesterol plasma levels (r = –0.46, p < 0.05), and within the group of TH CRF patients the IBS index was also negatively correlated with the body mass index and diastolic blood pressure. The carotid intima-media thickness was similar between uremic patients and controls. This study demonstrates an increment in carotid ultrasonic reflectivity in CRF patients, independent of the presence of overt atherosclerotic damage, and probably related to vascular remodelling linked to CRF. IBS analysis can be a useful tool to detect early changes in arterial wall structure. However, prospective studies should be planned to define its prognostic importance in uremic patients.

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          Chronic renal failure--a vasculopathic state.

           R K Luke (1998)
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            Alterations of Arterial Function in End-Stage Renal Disease

            Cardiovascular disease is a major cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Epidemiological and clinical studies have shown that this is most frequently related to damage of large conduit arteries. Macrovascular disease develops rapidly in uremic patients and is responsible for the high incidence of ischemic heart disease, sudden death, peripheral artery diseases, and congestive heart failure. The most frequent causes of these complications are occlusive lesions due to atherosclerosis. Nevertheless, atherosclerosis, a disease characterized by the presence of plaques, represents only one form of structural response to metabolic and hemodynamic alterations which interfere with the process of aging, i.e., arteriosclerosis, characterized by dilation/hypertrophy and stiffening of arteries. The vascular complications in ESRD are ascribed to two different but associated mechanisms, namely atherosclerosis and arteriosclerosis. Whereas the former principally affects the conduit function with ischemic lesions being the most characteristic consequence, the latter primarily disturbs the cushioning function of large arteries. Arteriosclerosis in ESRD patients is characterized by diffuse dilation and hypertrophy of large conduit arteries and stiffening of arterial walls and represents a clinical form of accelerated aging process. The main clinical characteristics of arterial stiffening concern changes in blood pressure with isolated increase in systolic pressure and normal or lower diastolic pressure. The consequences of these alterations are: (1) an increased left ventricular afterload with development of left ventricular hypertrophy and increased myocardial oxygen demand and (2) altered coronary perfusion and subendocardial blood flow distribution. Epidemiological studies have identified arterial remodeling and stiffening as independent predictors of overall and cardiac mortality in ESRD patients.
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              Oxidant Stress in Hemodialysis


                Author and article information

                S. Karger AG
                June 2002
                03 June 2002
                : 91
                : 2
                : 270-275
                Department of Internal Medicine, University of Pisa, Italy
                58403 Nephron 2002;91:270–275
                © 2002 S. Karger AG, Basel

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                Figures: 4, Tables: 2, References: 23, Pages: 6
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