首页> 中文期刊> 《微循环学杂志》 >慢性肾脏病患者血清半乳糖凝集素3水平与动脉粥样硬化的关系

慢性肾脏病患者血清半乳糖凝集素3水平与动脉粥样硬化的关系

         

摘要

目的:分析慢性肾脏疾病(CKD)患者血清半乳糖凝集素-3(Gal-3)水平变化与动脉粥样硬化(AS)的关系.方法:选取我院2014-05-2016-01在肾内科就诊且未行透析治疗的CKD患者(CKD组)及同期体检健康者(对照组)各68例,CKD组患者又按不同临床分期分为1期组(n=l4)、2期组(n=18)、3期组(n=20)、4期组(n=9)、5期组(n=7).对所有人选者进行血液学检查,包括血清Gal-3检测;对CKD患者行颈动脉超声检查颈动脉内-中膜厚度(IMT)、统计斑块检出率及动脉硬化发生率.比较各组血液学指标的差异以及不同临床分期CKD患者Gal-3水平、颈动脉超声结果的差异.结果:CKD组患者血清中的Gal-3水平明显的低于对照组;血肌酐(SCr)、血尿素氮(BUN)、血清胱抑素C(CySC)水平与对照组相比显著增高,差异有统计学意义(P<0. 05).随着CKD分期的逐渐加重,CKD 5期患者的血清Gal-3水平显著的高于1-4期患者(P<0. 05).各期CKD组患者的颈动脉超声检查结果比较差异有统计学意义,且随着分期的加重,颈动脉ITM、ITM增厚例数及斑块检出率、动脉硬化发生例数增加的趋势,差异有统计学意义(P<0. 05).结论:血清Gal-3水平降低与CKD患者临床分期及AS形成相关.%Objective: To discuss the relationship between serum galectin-3(Gal-3) and AS in chronic kidney disease. Method: 68 patients with non-dialytic chronic kidney disease(CKD) and 68 patients with healthy check-up from May 2014 to January 2016 were enrolled. According to different clinical stages the CKD group patients were divided into 1 group (n= 14), 2 group (n= 18), 3 group (n = 20), 4 group (n = 9), 5 group (n = 7). Hematological examination was performed for all selected patients, including serum Gal-3 test; Carotid ultrasonography in CKD patients, including carotid IMT, plaque detection rate and arteriosclerosis incidence. The differences of hematological indexes and Gal-3 levels in CKD patients with different clinical stages and carotid artery ultrasound were analyzed. Results: Serum Gal-3 level in CKD group were significantly lower than the control group; Serum Cr, BUN, CysC levels were significantly higher than the control group, P<0. 05. With the gradual increase of CKD stage, serum Gal-3 levels in patients with CKD phase 5 were significantly higher than phase 1-4 (P<0. 05). The results of carotid ultrasonography in CKD group showed statistically significant difference, and with CKD staging getting worse, the incidence of carotid ITM and plaque detection rate and atherosclerosis increased, (P<0. 05). Conclusion: Serum Gal-3 level decreased was associated with clinical stage and AS formation in CKD patients.

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