Objective. To identify the relationship between microinflammation, oxidative stress, and carotid arterial stiffness in hemodialysis patients. Methods. The CAS β and PWV obtained by ultrasound technology were used to assess carotid arterial stiffness. We divided the patients into either the CAS group or the non-CAS group based on the presence or absence of CAS. The parameters of ALB, Ca, P, TC, HDL, LDL, TG, glucose, creatinine, and hs-CRP levels were routinely tested in both groups of patients. The levels of TNF-α, IL-6, and 8-isoprostane F2α were measured by ELISA. Results. A total of 42 patients were enrolled in the CAS group and 20 patients were enrolled in the non-CAS group. No significant differences between the CAS group and the non-CAS group were observed with respect to age, dialysis duration, DBP, BUN, Cr, TC, TG, HDL, LDL, and Hb. However, SBP , pulse pressure, and 8-isoprostane levels of the CAS group were higher than those of the non-CAS group. The hs-CRP, TNF-α, and IL-6 levels were elevated in both groups but showed no significant differences. Conclusions. Maintenance of hemodialysis patients exhibits a microinflammatory state that may lead to atherosclerosis. The roles of hypertension and oxidative stress may be more important. 1. Introduction Atherosclerosis is an independent predictor of cardiovascular disease (CVD) related to patients with end-stage renal disease (ESRD). Numerous factors are involved in atherosclerosis for ESRD patients, some of which are reversible. Increasing evidence has demonstrated that atherosclerosis is a chronic microinflammatory disease [1–4]. Renal excretion dysfunction is common for maintenance with hemodialysis (MHD) patients. Toxins and cytokines accumulate in the body. The imbalance between the antioxygen free radical system and the oxygen free radical production system causes peroxidative damage and lipid peroxidative injury. Glycation end products and advanced oxidation protein products accumulate in the body, bind to specific monocyte-macrophage cell surface receptors, and stimulate vast numbers of adhesion molecules. Nuclear factor κB (NF-κB) is also stimulated resulting in increased secretion of inflammatory cytokines such as interleukin (IL) 1, IL-6, and tumor necrosis factor (TNF) α [5, 6]. Inflammatory cytokines and oxidative stress play an important role in dialysis-related cardiovascular events in MHD patients [7, 8]. In previous studies, systolic blood pressure (SBP), age, increased blood calcium (Ca) levels, and diabetes were demonstrated to be independent risk factors for carotid artery
References
[1]
J. Blacher, M. E. Safar, B. Pannier, A. P. Guerin, S. J. Marchais, and G. M. London, “Prognostic significance of arterial stiffness measurements in end-stage renal disease patients,” Current Opinion in Nephrology and Hypertension, vol. 11, no. 6, pp. 629–634, 2002.
[2]
M. Briet, E. Bozec, S. Laurent et al., “Arterial stiffness and enlargement in mild-to-moderate chronic kidney disease,” Kidney International, vol. 69, no. 2, pp. 350–357, 2006.
[3]
P. Tseke, E. Grapsa, K. Stamatelopoulos et al., “Atherosclerotic risk factors and carotid stiffness in elderly asymptomatic HD patients,” International Urology and Nephrology, vol. 38, no. 3-4, pp. 801–809, 2006.
[4]
J. Blacher, B. Pannier, A. P. Guerin, S. J. Marchais, M. E. Safar, and G. M. London, “Carotid arterial stiffness as a predictor of cardiovascular and all- cause mortality in end-stage renal disease,” Hypertension, vol. 32, no. 3, pp. 570–574, 1998.
[5]
S. Kato, M. Chmielewski, H. Honda et al., “Aspects of immune dysfunction in end-stage renal disease,” Clinical Journal of the American Society of Nephrology, vol. 3, no. 5, pp. 1526–1533, 2008.
[6]
S. Shahrokh, P. Heydarian, F. Ahmadi, F. Saddadi, and E. Razeghi, “Association of inflammatory biomarkers with metabolic syndrome in hemodialysis patients,” Renal Failure, vol. 34, pp. 1109–1113, 2012.
[7]
E. Dounousi, E. Papavasiliou, A. Makedou et al., “Oxidative stress is progressively enhanced with advancing stages of ckd,” American Journal of Kidney Diseases, vol. 48, no. 5, pp. 752–760, 2006.
[8]
I. Karamouzis, P. A. Sarafidis, M. Karamouzis et al., “Increase in oxidative stress but not in antioxidant capacity with advancing stages of chronic kidney disease,” American Journal of Nephrology, vol. 28, no. 3, pp. 397–404, 2008.
[9]
H.-Q. Ren, Y. Li, Q. Cai, S.-J. Han, M.-Y. Lv, and L. Li, “Determinants of arterial distensibility in middle-age and elderly patients on the treatment of hemodialysis,” Chinese Journal of Emergency Medicine, vol. 19, no. 10, pp. 1070–1073, 2010.
[10]
H. Q. Ren, G. Chen, Q. Cai, Y. Li, S. Han, and L. Li, “Risk factors for carotid artery distensibility in middle-aged and elderly hemodialysis patients,” World Journal of Emergency Medicine, vol. 2, pp. 137–140, 2011.
[11]
E. C. Godia, R. Madhok, J. Pittman et al., “Carotid artery distensibility: a reliability study,” Journal of Ultrasound in Medicine, vol. 26, no. 9, pp. 1157–1165, 2007.
[12]
H. P. Zhang, X. H. Wang, and K. G. Zhan, “Evaluation of the carotid artery elasticity of the eldely with hypertension only using echo-tracking technique,” Journal of Medical Imaging, vol. 19, pp. 1113–1115, 2009.
[13]
Y. L. Zhou, Z. X. Yu, and H. M. Jia, “Association of insulin resistance with common carotid arterial stiffness in hemodialysis patients,” Chinese Journal of Nephrology, vol. 24, pp. 249–252, 2008.
[14]
G. A. Kaysen, “The microinflammatory state in uremia: causes and potential consequences,” Journal of the American Society of Nephrology, vol. 12, no. 7, pp. 1549–1557, 2001.
[15]
A. Merino, S. Nogueras, P. Buendía et al., “Microinflammation and endothelial damage in hemodialysis,” Contributions to Nephrology, vol. 161, pp. 83–88, 2008.
[16]
G. Garibotto, A. Sofia, V. Procopio et al., “Peripheral tissue release of interleukin-6 in patients with chronic kidney diseases: effects of end-stage renal disease and microinflammatory state,” Kidney International, vol. 70, no. 2, pp. 384–390, 2006.
[17]
R. Pouresmaeil, E. Razeghi, and F. Ahmadi, “Correlation of serum lead levels with inflammation, nutritional status, and clinical complications in hemodialysis patients,” Renal Failure, vol. 34, pp. 1114–1117, 2012.
[18]
I. Karamouzis, D. Grekas, M. Karamouzis et al., “Enhanced oxidative stress with a gradient between plasma and muscle interstitial fluid in patients with end stage renal failure on hemodialysis,” Hormones, vol. 7, no. 1, pp. 62–69, 2008.
[19]
J. W. Groothoff, M. P. Gruppen, M. Offringa et al., “Increased arterial stiffness in young adults with end-stage renal disease since childhood,” Journal of the American Society of Nephrology, vol. 13, no. 12, pp. 2953–2961, 2002.
[20]
D. Sollinger, M. G. Mohaupt, A. Wilhelm, D. Uehlinger, F. J. Frey, and U. Eisenberger, “Arterial stiffness assessed by digital volume pulse correlates with comorbidity in patients with ESRD,” American Journal of Kidney Diseases, vol. 48, no. 3, pp. 456–463, 2006.
[21]
J. N. Cohn, “Arteries, myocardium, blood pressure and cardiovascular risk: towards a revised definition of hypertension,” Journal of Hypertension, vol. 16, no. 12, pp. 2117–2124, 1998.