Liu Bi-cheng, Li Li, Gao Min, Wang Yan-li, Yu Ji-rong
Institute of Nephrology, Zhong Da Hospital, Southeast University, Nanjing, Jiangsu 210009, China.
Chin Med J (Engl). 2008 Nov 5;121(21):2157-61.
Vascular access (VA) dysfunction is a major clinical complication in the hemodialysis population and has a direct effect on dialysis outcome. This study was conducted to explore the role of microinflammation in the VA dysfunction in maintenance hemodialysis patients.
Forty-seven patients (male 35 and female 12) receiving maintenance hemodialysis were included for this study. They were divided into three groups: group 1 (n = 15), patients with initial hemodialysis and new arteriovenous fistula (AVF); group 2 (n = 18), patients treated with hemodialysis for long term with well-functional VA; group 3 (n = 14), maintenance hemodialysis patients with VA dysfunction. Biochemical parameters and serum tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) were determined. High-sensitivity C-reactive protein (hs-CRP) was determined by latex-enhanced immuno-nephelometric method. Tissues of radial artery were taken from group 1 and group 3 for the histological study. Expression of CD68 and MCP-1 in the radial artery was determined by immunohistochemistry.
Serum hs-CRP in group 3 was significantly higher than those in group 1 and group 2 ((7.40 +/- 2.42) mg/L vs (4.21 +/- 1.62) mg/L and (5.04 +/- 3.65) mg/L, P < 0.01 and P < 0.05, respectively). Serum TNF-alpha in group 3 was significantly higher than those in group 1 and group 2 ((64.03 +/- 9.29) pg/ml vs (54.69 +/- 12.39) pg/ml and (54.05 +/- 7.68) pg/ml, P < 0.05 and P < 0.01, respectively). Serum IL-6 in group 3 was also significantly higher than those in group 1 and group 2 ((70.09 +/- 14.53) pg/ml vs (56.43 +/- 10.11) pg/ml and (60.77 +/- 9.70) pg/ml, P < 0.01 and P < 0.05, respectively). Patients in group 3 had a thicker internal layer of vessels than in group 1 ((0.356 +/- 0.056) mm vs (0.111 +/- 0.021) mm, P < 0.01). Expression of CD68 and MCP-1 in the fistula vessel walls in group 3 were much higher than those in group 1 (P < 0.01). Moreover, serum hs-CRP level was positively correlated with the neointimal hyperplasia, the expression of CD68 and MCP-1 in fistula vessel (P < 0.01, respectively).
Microinflammation might be involved in the dysfunction of AVF in patients with maintenance hemodialysis.
血管通路（VA）功能障碍是血液透析人群中的主要临床并发症，对透析结果有直接影响。本研究旨在探讨微炎症在维持性血液透析患者VA功能障碍中的作用。
本研究纳入47例接受维持性血液透析的患者（男性35例，女性12例）。他们被分为三组：第1组（n = 15），初次血液透析且有新动静脉内瘘（AVF）的患者；第2组（n = 18），长期接受血液透析且VA功能良好的患者；第3组（n = 14），有VA功能障碍的维持性血液透析患者。测定生化参数以及血清肿瘤坏死因子-α（TNF-α）、白细胞介素6（IL-6）和单核细胞趋化蛋白-1（MCP-1）。采用乳胶增强免疫比浊法测定高敏C反应蛋白（hs-CRP）。从第1组和第3组获取桡动脉组织进行组织学研究。采用免疫组织化学法测定桡动脉中CD68和MCP-1的表达。
第3组血清hs-CRP显著高于第1组和第2组（分别为(7.40 ± 2.42)mg/L vs (4.21 ± 1.62)mg/L和(5.04 ± 3.65)mg/L，P < 0.01和P < 0.05）。第3组血清TNF-α显著高于第1组和第2组（分别为(64.03 ± 9.29)pg/ml vs (54.69 ± 12.39)pg/ml和(54.05 ± 7.68)pg/ml，P < 0.05和P < 0.01）。第3组血清IL-6也显著高于第1组和第2组（分别为(70.09 ± 14.53)pg/ml vs (56.43 ± 10.11)pg/ml和(60.77 ± 9.70)pg/ml，P < 0.01和P < 0.05）。第3组患者血管内层比第1组更厚（分别为(0.356 ± 0.056)mm vs (0.111 ± 0.021)mm，P < 0.01）。第3组瘘管壁中CD68和MCP-1的表达远高于第1组（P < 0.01）。此外，血清hs-CRP水平与瘘管新生内膜增生、CD68和MCP-1在瘘管血管中的表达呈正相关（分别为P < 0.01）。
微炎症可能参与维持性血液透析患者AVF的功能障碍。
