Endogenous soluble receptor of advanced glycation end-products (esRAGE) is negatively associated with vascular calcification in non-diabetic hemodialysis patients

被引:5
作者
NasrAllah M.M. [1 ]
El-Shehaby A.R. [2 ]
Osman N.A. [1 ]
Salem M.M. [3 ]
Nassef A. [4 ]
Sharaf El Din U.A.A. [1 ,5 ]
机构
[1] Department of Nephrology, Kasr El-Aini School of Medicine, Cairo University, Cairo
[2] Department of Medical Biochemistry, Kasr El-Aini School of Medicine, Cairo University, Cairo
[3] Department of Endocrinology, Kasr El-Aini School of Medicine, Cairo University, Cairo
[4] Department of Radiology, Kasr El-Aini School of Medicine, Cairo University, Cairo
[5] Department of Nephrology, Kasr El-Aini School of Medicine, Cairo University and International Kidney Centre, Cairo
关键词
Advanced glycation end-products; CKD-MBD; HsCRP; Inflammation; RAGE; Vascular calcification;
D O I
10.1007/s11255-011-0007-x
中图分类号
学科分类号
摘要
Background: Advanced glycation end-products (AGE) accumulate in CKD and may predispose to cardiovascular disease by inducing inflammatory and oxidant stress in the vascular endothelium. Soluble forms of the receptor for AGE (RAGE) may be protective against these effects by binding AGE in the soluble phase. Accumulating evidence suggests a protective role of soluble RAGE against vascular calcification. This study investigates the association between endogenous soluble RAGE (esRAGE) and vascular calcification in hemodialysis patients. Methods: We studied 65 non-diabetic hemodialysis patients, on 3 9 4 h dialysis schedule, and 19 controls. Serum levels of esRAGE, hsCRP, parathormone, lipids, calcium, and phosphorus were measured. Aortic calcification index (ACI) was measured using non-contrast CT of the abdominal aorta. Results: Aortic calcification was detected in 64 out of 65 hemodialysis patients. Levels of esRAGE were lower in hemodialysis patients (278 pg/ml, SD 101.1) than in controls (443 ± 109 pg/ml; P = 0.001). ACI correlated negatively in stepwise multivariate analysis with esRAGE (P = 0.002) and positively with hsCRP (<0.0001), systolic blood pressure (P<0.0001) and dialysis vintage (P = 0.05); R2 = 0.65. Conclusion: Levels of esRAGE were low among hemodialysis patients and correlated negatively with ACI. © Springer Science+Business Media, B.V. 2011.
引用
收藏
页码:1193 / 1199
页数:6
相关论文
共 37 条
  • [11] Yan S.F., Ramasamy R., Schmidt A.M., Soluble RAGE: Therapy and biomarker in unraveling the RAGE axis in chronic disease and aging, Biochem Pharmacol, 79, pp. 1379-1386, (2010)
  • [12] Basta G., Leonardis D., Mallamaci F., Et al., Circulating soluble receptor of advanced glycation end product inversely correlates with atherosclerosis in patients with chronic kidney disease, Kidney Int, 77, pp. 225-231, (2010)
  • [13] Vazzana N., Santilli F., Cuccurullo C., Et al., Soluble forms of RAGE in internal medicine, Intern Emerg Med, 4, pp. 389-401, (2009)
  • [14] Basta G., Receptor for advanced glycation endproducts and atherosclerosis: From basic mechanisms to clinical implications, Atherosclerosis, 196, pp. 9-21, (2008)
  • [15] Katakami N., Matsuhisa M., Kaneto H., Et al., Serum endogenous secretory RAGE level is an independent risk factor for the progression of carotid atherosclerosis in type 1 diabetes, Atherosclerosis, 204, pp. 288-292, (2009)
  • [16] Choi K.M., Yoo H.J., Kim H.Y., Et al., Association between endogenous secretory RAGE, inflammatory markers and arterial stiffness, Int J Cardiol, 132, pp. 96-101, (2009)
  • [17] Nishizawa Y., Koyama H., Endogenous secretory receptor for advanced glycation end-products and cardiovascular disease in end-stage renal disease, J Ren Nutr, 18, pp. 76-82, (2008)
  • [18] Koyama H., Yamamoto H., Nishizawa Y., Endogenous secretory RAGE as a novel biomarker for metabolic syndrome and cardiovascular diseases, Biomark Insights, 2, pp. 331-339, (2007)
  • [19] Yamagishi S., Fujimori H., Yonekura H., Et al., Advanced glycation endproducts accelerate calcification in microvascular pericytes, Biochem Biophys Res Commun, 258, pp. 353-357, (1999)
  • [20] Ren X., Shao H., Wei Q., Et al., Advanced glycation end-products enhance calcification in vascular smooth muscle cells, J Int Med Res, 37, pp. 847-854, (2009)