慢性肾脏病患者脂联素水平与相关因素研究
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摘要
目的探讨慢性肾脏病(CKD)各期患者体内脂联素、氧化应激、微炎症状态及营养水平,研究其之间的相互关系。
方法选择近期无感染、创伤、心脑血管事件、糖尿病及尿蛋白阳性的CKDⅠ～Ⅱ期、Ⅲ期、Ⅳ期及Ⅴ期的HD和PD患者各20例为试验组(诊断及分期按K/DOQI指南2003版标准);选择肾功能正常的肿瘤患者20例为疾病对照组,体检健康成年人20例为健康对照组。应用酶联免疫吸附法测定外周血脂联素(APN)和高敏C反应蛋白(hs-CRP)、白介素-6(IL-6)含量。用TBA法测定血清丙二醛(MDA)含量。常规检测血清BUN、Cr、HB、Alb、Pro-Alb、TG、CH、HDL、LDL及Lp-α含量。用主观综合性营养评估法(SGA)评估所有入选者的营养状况。SPSS15.0软件包进行数据分析,组间比较用t检验,两组指标相关性用直线相关分析,P＜0.05表示有统计学意义。
结果CKD各期组的APN、hs-CRP和MDA水平均高于正常对照组,ALB水平均低于正常对照组(P＜0.05和P＜0.01);IL-6水平在CKDⅢ-Ⅴ期均高于正常对照组(P＜0.01)。Pro-ALB水平在CKDⅣ、Ⅴ期均低于正常对照组(P＜0.01)。CKD各期和疾病对照组以及正常对照组之间SGA评估无明显差异,但在CKD各期间随病情进展营养不良逐渐加重。APN、IL-6、hs-CRP、MDA之间存在正相关,r值范围为0.215～0.515(P＜0.05):APN、IL-6、MDA与HB、ALB、Pro-ALB之间呈负相关,r值范围为-0.203～-0.614(P＜0.05)。
结论1.APN水平升高和氧化应激、微炎症状态、营养不良贯穿于CKD发展的全过程,并随着肾功能的减退,逐渐增强。2.CKD患者体内氧化应激、微炎症状态和营养不良相互促进,形成心血管事件发生的高危环境。3.在此高危环境下,APN反应性升高,氧化应激、微炎症状态和营养不良是导致CKD患者APN水平升高的重要因素。
Objective To investigate the level of adiponectin、oxidative stress,microinflammation and malnutrition on the patients of every stage of chronic kidney disease(CKD),and analyze their correlativity.
Methods Without infection,wound,cardiocerebrovascular events,diabetes and albuminuria, 20 of every stage of CKD(following the K/DOQI guide) patients were enrolled in the study.20 of tumor patients with normal renal function were enrolled as disease control group.20 of health adults were enrolled as normal conctrol group.The serum levels of adiponectin(APN),Interleukin-6 (IL-6)、hs-C-reaction protein(hs-CRP) were measured by enzyme linked immunosorbent assay (ELISA).The serum level of Malondialdehyde(MDA) was tested by thio-barbituric acid(TBA),and tested levels of BUN、Cr,Alb、Pro-Alb、TG、CH、HDL、LDL、Lp-a and HB.Subjective global assessment of nutritional status(SGA) was used to evaluate patients'nutritional status.SPSS15.0 statistics software were applied to analyze the data.
Result The levels of APN、hs-CRP and MDA in each CKD group were higher,and the serum ALB concentration was lower,compared with those of normal control group(P＜0.05 or P＜0.01).The levels of IL-6(CKDⅢ～Ⅴgroup)were higher and the levels of Pro-ALB(CKDⅣandⅤgroup) were lower,compared with normal control group(P＜0.01).There was no difference between all the groups in SGA,but the degree of malnutrition was higher and higher.There were positively correlations between APN、IL-6、hs-CRP and MDA(r=0.215～0.515,P＜0.05 ),and negatively correlation between APN,IL-6、MDA and HB、ALB、Pro-ALB(r=-0.203～0.614,P＜0.05).
Conclusion 1.There are high APN and oxidative stress、microinflammation、malnutrition in all stages of CKD development,and it become higher and higher,following renal function' decrease.2. Oxidative stress、microinflammation and malnutrition form an dangerous environment for cardiovascular events.3.In the environment,APN reactively increase,and oxidative stress、microinflammation,malnutrition are the main causes.
方法选择近期无感染、创伤、心脑血管事件、糖尿病及尿蛋白阳性的CKDⅠ～Ⅱ期、Ⅲ期、Ⅳ期及Ⅴ期的HD和PD患者各20例为试验组(诊断及分期按K/DOQI指南2003版标准);选择肾功能正常的肿瘤患者20例为疾病对照组,体检健康成年人20例为健康对照组。应用酶联免疫吸附法测定外周血脂联素(APN)和高敏C反应蛋白(hs-CRP)、白介素-6(IL-6)含量。用TBA法测定血清丙二醛(MDA)含量。常规检测血清BUN、Cr、HB、Alb、Pro-Alb、TG、CH、HDL、LDL及Lp-α含量。用主观综合性营养评估法(SGA)评估所有入选者的营养状况。SPSS15.0软件包进行数据分析,组间比较用t检验,两组指标相关性用直线相关分析,P＜0.05表示有统计学意义。
结果CKD各期组的APN、hs-CRP和MDA水平均高于正常对照组,ALB水平均低于正常对照组(P＜0.05和P＜0.01);IL-6水平在CKDⅢ-Ⅴ期均高于正常对照组(P＜0.01)。Pro-ALB水平在CKDⅣ、Ⅴ期均低于正常对照组(P＜0.01)。CKD各期和疾病对照组以及正常对照组之间SGA评估无明显差异,但在CKD各期间随病情进展营养不良逐渐加重。APN、IL-6、hs-CRP、MDA之间存在正相关,r值范围为0.215～0.515(P＜0.05):APN、IL-6、MDA与HB、ALB、Pro-ALB之间呈负相关,r值范围为-0.203～-0.614(P＜0.05)。
结论1.APN水平升高和氧化应激、微炎症状态、营养不良贯穿于CKD发展的全过程,并随着肾功能的减退,逐渐增强。2.CKD患者体内氧化应激、微炎症状态和营养不良相互促进,形成心血管事件发生的高危环境。3.在此高危环境下,APN反应性升高,氧化应激、微炎症状态和营养不良是导致CKD患者APN水平升高的重要因素。
Objective To investigate the level of adiponectin、oxidative stress,microinflammation and malnutrition on the patients of every stage of chronic kidney disease(CKD),and analyze their correlativity.
Methods Without infection,wound,cardiocerebrovascular events,diabetes and albuminuria, 20 of every stage of CKD(following the K/DOQI guide) patients were enrolled in the study.20 of tumor patients with normal renal function were enrolled as disease control group.20 of health adults were enrolled as normal conctrol group.The serum levels of adiponectin(APN),Interleukin-6 (IL-6)、hs-C-reaction protein(hs-CRP) were measured by enzyme linked immunosorbent assay (ELISA).The serum level of Malondialdehyde(MDA) was tested by thio-barbituric acid(TBA),and tested levels of BUN、Cr,Alb、Pro-Alb、TG、CH、HDL、LDL、Lp-a and HB.Subjective global assessment of nutritional status(SGA) was used to evaluate patients'nutritional status.SPSS15.0 statistics software were applied to analyze the data.
Result The levels of APN、hs-CRP and MDA in each CKD group were higher,and the serum ALB concentration was lower,compared with those of normal control group(P＜0.05 or P＜0.01).The levels of IL-6(CKDⅢ～Ⅴgroup)were higher and the levels of Pro-ALB(CKDⅣandⅤgroup) were lower,compared with normal control group(P＜0.01).There was no difference between all the groups in SGA,but the degree of malnutrition was higher and higher.There were positively correlations between APN、IL-6、hs-CRP and MDA(r=0.215～0.515,P＜0.05 ),and negatively correlation between APN,IL-6、MDA and HB、ALB、Pro-ALB(r=-0.203～0.614,P＜0.05).
Conclusion 1.There are high APN and oxidative stress、microinflammation、malnutrition in all stages of CKD development,and it become higher and higher,following renal function' decrease.2. Oxidative stress、microinflammation and malnutrition form an dangerous environment for cardiovascular events.3.In the environment,APN reactively increase,and oxidative stress、microinflammation,malnutrition are the main causes.
引文
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13. Lindsay RS, Funahashi T, Krakoff J, et al. Genome wide linkage analysis of serum adiponectin in the Pima India population. Diabetes, 2003, 52(9):2419-2425
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15. Kern PA , Di Gregorio GB , Lu T, Rassouli N , Ranganathan G. Adiponectin expression from human adipose tissue relation to obesity , insulin resistance , and tumor necrosis factor-α expression. Diabtes ,2003 , 52(7): 1779-1785
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19.Matsubara M,Namioka K,Katayose S.Decreased plasma adiponectin concentrations in women with low grade creactive protein elevation.ERr J Endocrino1,2003,148(6):657-662
20.Hulthe J,Uulten LM,Fagerberg B.Low adipocyte derived plasma protein adiponectin concentrantions are associated with the metabolic syndrome and small dense low-density liporotein particles:Atherosclerosis and insulin resistance study.Metabolism,2003,52(12):1612-1614
21.Adamczak M,Wiecek A,Funahashi T,et al.Decreasde plasma adiponectin concentration in patients with essential hypertension.Am J Hypertens,2003,16(1):72-75
22.Stefan N,Stumuvoll M,Vozarova B,et al.Plasma adiponectin and endogenous glucose production in humans.Diabetes Care,2003,26(12):3315-3319
23.林泽鹏,徐明星,方卫华.原发性高血压患者血清脂联素浓度的变化及肾素-血管紧张素系统对其影响.中国循环杂志,2004,19(3):205-208
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26.Quchi N,iihara S,Funahashi T,et al.Reciprocal association of C-reactive protein with adiponectin in blood stream and adipose tissue.Circulation,2003,107(5):671-674
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27.Manigrasso MR,Ferroni P,Santilli F,et al.hssociation between circulating adiponectin and interleukin-10 levels in android obesity:effect of weight loss.J Clin Endocrinol Metab,2005,90:5876-5879
28.Wolf AM,Wolf D,Rumpold H,et al.Adiponectin induces the anti-inflammatory cytokines IL-10 and IL-1RA in human leukocytes.Biochem Biophys Res Commun,2004,323:630-635
29.Ajuwong KM,SpurlockME.Adiponectin inhibits LPS-induced NF-kB activation and IL-6production and increases PPAR- γ 2 exprssion in aipocytes,Am J Physiol Rrgul Integr Comp Physiol,2005,288:1220- 1225
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31.Ouchi N,Kihara S,Arita Y,etal.Novel modulator for endothelial adhesion molecules:adipocyte-derived plasma protein adiponectin.Circulation,1999,100(25):2473-2476
32.Chudek J,Adamczak M,Karkoszka H,et al.Plasma adiponectin concentration before and after successful kidney transplantataion.Transplant Proc,2003,35:2186-2189
33.Zoccali C,Mallomaci F,panuccioV,et al.Adiponectin is markedly increased in patients with nephrotic syndrome and is related to metabolic risk factors.Kidney Int,(suppl),2003,(84),98-102
34.张庆芳,任野平,张蕊等.慢性肾衰患者血清脂联素水平及其临床意义的研究.哈尔并医科大学学报,2005,39(6):505-507
35.Zoccali C.et al.Adiponectin,metabolic risk factors,and cardiovascular events among patients with end-stage-renal-disease.J Am Soc Nephrol.2002,13(1):134-141
36.Hotamisligil GS,Arnerp,Caro JF.Increased adipose tissue expression of tumor necrosis factor- α in human obesityand insulin resistance.Clin Lnvtst,1995,95,2409 -2415
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