慢性肾脏病患者血清瘦素水平与微炎症反应的关系及其在动脉粥样硬化中的作用
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摘要
目的:1.探讨慢性肾脏病(CKD)患者血清瘦素和C-反应蛋白浓度的改变;2.探讨慢性肾脏病患者颈动脉内膜-中层厚度(IMT)的变化;3.探讨慢性肾脏病患者血清瘦素水平与C-反应蛋白水平及临床各指标之间的关系;4.探讨慢性肾脏病患者血清瘦素和C-反应蛋白与颈动脉IMT的相关性和两者在动脉粥样硬化发生中的可能机制。
方法:收集我科住院的CKD患者79例,男51例,女28例,平均年龄44.22±13.47岁。CKD诊断标准参照K/DOQI指南[1]。原发病包括:慢性肾小球肾炎58例、多囊肾3例、梗阻性肾病6例、慢性小管间质性肾炎5例、病因不明7例。按照GFR水平分为3组: (1)CKD2~3期26例(GFR30~89ml/min/1.73m2),其中男性18例,女性8例,平均年龄44.69±14.13岁;(2)CKD4期22例(GFR15~29 ml/min/1.73m2),其中男性16例,女性6例,平均年龄42.7±12.63岁;(3)CKD5期31例(GFR<15ml /min/1.73m2),其中男性17例,女性14例,平均年龄45.19±13.78岁;(4)健康对照组13例,其中男性8例,女性5例,平均年龄40.07±18.51岁。排除标准:①近1个月内感染、手术、创伤者;②近1个月发生过急性心血管事件者;③近六个月内使用过激素和免疫抑制剂者;④合并恶性肿瘤、妊娠者;⑤糖尿病肾病;⑥进入透析的患者或者肾移植患者。所有受试者于清晨空腹卧位抽取肘静脉血6ml,应用全自动生化分析仪测定常规生化指标,其中包括同时测定临床生化指标,其中包括血常规(Rt)、血清肌酐(Scr)、尿素氮(BUN)、血糖、总胆固醇(Chol)、甘油三酯(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)、极低密度脂蛋白(VLDL)、血清总蛋白(TP)和白蛋白(Alb)。同时离心分离血清,置-70℃保存备检,用时冰融,集中测定瘦素和CRP。血清瘦素(leptin)浓度测定应用放射免疫分析法,血清高敏CRP(hs-CRP)采用免疫透射比浊法。采用高分辨超声技术测颈动脉内膜-中层厚度(IMT)及粥样硬化斑块。计算体质量指数(BMI)[BMI=体质量(kg)/身高(m)2]和肾小球滤过率(GFR)。
结果:1.慢性肾脏病患者的血清瘦素水平(14.86±5.92 ng/L)明显高于健康对照组(8.72±2.35ng/m1)p<0.01,且随肾功能恶化逐渐升高(CKD2~3期:12.0±2.56ng/ml;CKD4期:14.98±5.69ng/ml;CKD5期:19.78±5.23ng/ml)。慢性肾脏病患者的血清C-反应蛋白水平(2.65±1.32mg/L)明显高于健康对照组(1.52±0.88mg/L) p<0.01,且随肾功能恶化逐渐升高(CKD2~3期:1.85±0.86mg/L;CKD4期:2.96±0.99mg/L;CKD5期:3.55±1.26 mg/L);2.慢性肾脏病患者的颈动脉IMT水平(0.953±0.256mm)明显高于健康对照组(0.675±0.249mm)p<0.01,且随肾功能恶化逐渐升高(CKD2~3期:0.681±0.172mm;CKD4期:0.814±0.173mm;CKD5期:0.932±0.156mm);3.慢性肾脏病患者颈动脉超声异常组(IMT增厚:颈总动脉IMT≥0.9mm,或分叉处IMT>0.9mm;粥样斑块:突向管腔的局灶性动脉壁增厚,其厚度超过相邻区域IMT至少50%)血清瘦素水平(17.06±1.06ng/ml)和CRP水平(3.32±0.19mg/L)较颈动脉正常组血清瘦素水平(14.27±0.70ng/ml)和CRP(2.55±0.17mg/L)明显升高;4.慢性肾脏病患者高CRP组血清瘦素水平(18.78±5.52ng/ml)和颈动脉IMT(0.79±0.19mm)较CRP正常组血清瘦素水平(14.20±5.17ng/ml)和颈动脉IMT(0.70±0.15mm)明显升高;5.慢性肾脏病患者高瘦素组血清CRP水平(3.66±0.21mg/L)和颈动脉IMT(0.79±0.133mm)较低瘦素组血清CRP水平(2.24g±0.14mg/L)和颈动脉(0.71±0.054mm)明显升高(P<0.05);6.慢性肾脏病患者存在营养不良者(ALB<35g/L)血清瘦素水平(16.67±0.93ng/ml)、血清C-反应蛋白浓度(3.14±0.21mg/L)和颈动脉IMT(0.760±0.273 mm)较ALB≥35g/L组血清瘦素水平(14.17±0.75ng/ml)、血清C-反应蛋白浓度(2.49±0.19mg/L)和颈动脉IMT(0.716±0.273mm)明显升高;7.慢性肾脏病患者的血清瘦素水平与临床各项指标的直线相关分析显示:①血清瘦素与尿素氮、肌酐、C-反应蛋白、体重指数之间呈显著正相关(r=0.293,P<0.01;r=0.324,P<0.01;r=0.539,P<0.01;r=0.312,P<0.05);②血清瘦素与肾小球滤过率、血红蛋白、ALB之间呈明显负相关(r=-0.389,P<0.01;r=-0.454,P<0.01;r=-0.246, P<0.05),与年龄、Chol、TG无明显相关性(r=0.014, P>0.05;r=0.051, P>0.05;r=-0.055, P>0.05);8.多元线性回归分析显示:CKD患者颈动脉IMT与血清瘦素、C-反应蛋白、甘油三脂、血红蛋白密切相关(β=0.546,P<0.01;β=0.386,P<0.05;β=0.791,P<0.05;β=0.532,P<0.01),提示血浆瘦素与C-反应蛋白直接参与了动脉粥样硬化、粥样斑块的形成;9. Logistic逐步回归分析显示:瘦素(β=1.527,95%CI:1.028~1.438,P<0.05)是CKD患者并发动脉粥样硬化的独立危险因素之一。
结论:①慢性肾脏病患者存在高瘦素血症和微炎症状态,②高瘦素血症与微炎症状态和慢性肾脏病患者高发动脉粥样硬化性心血管事件相关;③血清瘦素可能微炎症反应相互作用而参与了慢性肾脏病患者动脉粥样硬化的形成。
Objective : 1.To investigate the changes of the concentration of serum leptin and C-reaction protein (CRP) with chronic kidney disease (CKD);2.To investigate the changes of the level of IMT of carotid artery with chronic kidney disease(CKD);3.To investigate the relationship between the level of the serum leptin , C-reaction protein (CRP) and each of the parameter for clinic with chronic kidney disease (CKD);4.To explore the relationship among the serum leptin, C-reaction protein (CRP) and chronic kidney disease (CKD),and the possible mechanism of leptin to atherosclerosis seen in chronic kidney disease (CKD).
Methods:We collected 79 patients with chronic kidney disease (51 males and 28 females) aged 44.22±13.47 (mean±SD). The standard of diagnosis by using K/DOQI guideline[1]. The primary diseases: 53 patients were chronic glomerulo- nephritis, 5 patients were hypertention nephritis, 3 patients were polycystic kidney,4 patients were obstructive nephropathy and 12 patients were etiology unknown. 79 patients with chronic kidney disease were classified into three groups according to glomerular filtration rate (GFR): (1) CKD2~3 stage groups included 26 patients (GFR30~90ml/min /1.73m2), (18 males and 8 females),the average age is 44.69±14.13 years; (2) CKD4 stage groups included 22 patients (GFR15~30ml/min/1.73m2), (16 males and 6 females),the average age is 42.7±12.63 years;(3) CKD 5stage groups included 31 patients (GFR<15ml/min /1.73m2), (17 males and 14 females),the average age is 45.19±13.78 years;(4) Healthy control group included 13 healthy volunteers (8 males and 5 females), aged 40.07±18.51 (mean±SD). Excluding standards:①Those who were infected, operated on and had trauma in recently one month;②To have acute cardiovascular disease (CVD) in recently one month;③Those who have used the cortical hormone or other immunity conditioner in recently six months ;④To affiliate malignancy, pregnancy;⑤diabetic nephropathy;⑥To have dialysis or renal transplantation. All the patients starved for 12 hours and the vein blood 6ml was sampled in the morning. The blood samples were tested by the automatic biochemical machine to measure the blood routine, blood creatinine, urea nitrogen, blood sugar, the cholesterol, triglyceride, high dense lipoprotein cholesterol, low dense lipoprotein, very low density lipoproteintotal protein, albumin. At the same time, the serum was centrifugally separated and saved in -70℃refrigerator to measure the leptin and CRP, The leptin was tested by the radio-immunity method and the reagents were provided by the Beijing Puer Weiye Biotechnical Institute. The CRP was tested by the rate-scatter turbidimetry method and the antiserum was provided by Shanghai Sun Biotechnical Institute. Seventy nine CKD patients and 13 healthy volunteers were involved in the study. The serum leptin was tested by the radio-immunity method;The CRP was tested by the rate-scatter turbidimetry method. Intima-medial thickness (IMT) of extracranial common carotid artery and the presence of atherosclerotic plaques were determined by using noninvasive high-resolution B-mode ultrasonography. To calculate body mass index (BMI) and glomerular filtration rate (GFR).
Results:1. Levels of leptin in the chronic kidney disease (CKD) patients were significantly higher than those in the healthy groups, and to elevate along with the deteriorate of kidney function;Levels of CRP in the chronic kidney disease (CKD) patients were significantly higher than those in the healthy groups, and to elevate along with the deterioration of kidney function;2. The IMT in carotid artery were significantly higher in CKD patients compared with the healthy groups, and to elevate along with the deteriorate of kidney function;3. It was found that patients with chronic kidney disease in the high IMT of carotid artery groups had serum CRP and serum leptin concentrations significantly increased compared with the normal IMT of carotid artery groups;4. It was found that patients with chronic kidney disease in the high CRP groups had serum leptin concentrations and IMT of carotid artery significantly increased compared with the normal CRP groups;5. It was found that patients with chronic kidney disease in hyperleptin groups had serum CRP concentrations and IMT of carotid artery significantly increased compared with the lowleptin groups; 6. It was found that patients with chronic kidney disease in the Alb <35g/L groups had serum CRP concentrations and IMT of carotid artery significantly increased compared with the Alb >35g/L groups;7. The linear correlations were found between the leptin and parameters in patients with chronic kidney disease (CKD) as follows:①The serum leptin levels were correlated positively with urea nitrogen serum creatinine C-reaction body mass index (BMI) (r=0.293,P<0.01;r=0.324,P<0.01;r=0.539,P<0.01;r=0.312,P<0.05);②The serum leptin levels were correlated negatively with glomerular filtration rate hemoglobin albumin (r=-0.389,P<0.01;r=-0.454,P<0.01;r=-0.246, P< 0.05),and were not correlated with age cholesterol triglyceride (r=0.014, P>0.05;r=0.051, P>0.05;r=-0.055, P>0.05) 8.The linear correlation regression analyses for IMT and serum leptin, serum CRP, TG, Hb, showed that serum leptin and serum CRP participated straightly in the atherosclerosis of vessel and the forming of atherosclerosis spot mass. 9. Logistic regression analysis further indicated that Leptin (β=1.527, 95%CI :1.028~1.438 , P<0.05) was an independent risk factor of atherosclerosis-related cardiovascular events in chronic disease (CKD).
Conclusions:①There is hyperleptin and micro inflamma- tory state in the chronic kidney disease (CKD) patients.②The leptin and microinflammatory state might be in close correlation with atherosclerosis-related cardiovascular events in chronic kidney disease (CKD).③The serum leptin and microinflamma- tion may result in accelerated atherosclerosis seen in chronic kidney disease (CKD).
方法:收集我科住院的CKD患者79例,男51例,女28例,平均年龄44.22±13.47岁。CKD诊断标准参照K/DOQI指南[1]。原发病包括:慢性肾小球肾炎58例、多囊肾3例、梗阻性肾病6例、慢性小管间质性肾炎5例、病因不明7例。按照GFR水平分为3组: (1)CKD2~3期26例(GFR30~89ml/min/1.73m2),其中男性18例,女性8例,平均年龄44.69±14.13岁;(2)CKD4期22例(GFR15~29 ml/min/1.73m2),其中男性16例,女性6例,平均年龄42.7±12.63岁;(3)CKD5期31例(GFR<15ml /min/1.73m2),其中男性17例,女性14例,平均年龄45.19±13.78岁;(4)健康对照组13例,其中男性8例,女性5例,平均年龄40.07±18.51岁。排除标准:①近1个月内感染、手术、创伤者;②近1个月发生过急性心血管事件者;③近六个月内使用过激素和免疫抑制剂者;④合并恶性肿瘤、妊娠者;⑤糖尿病肾病;⑥进入透析的患者或者肾移植患者。所有受试者于清晨空腹卧位抽取肘静脉血6ml,应用全自动生化分析仪测定常规生化指标,其中包括同时测定临床生化指标,其中包括血常规(Rt)、血清肌酐(Scr)、尿素氮(BUN)、血糖、总胆固醇(Chol)、甘油三酯(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)、极低密度脂蛋白(VLDL)、血清总蛋白(TP)和白蛋白(Alb)。同时离心分离血清,置-70℃保存备检,用时冰融,集中测定瘦素和CRP。血清瘦素(leptin)浓度测定应用放射免疫分析法,血清高敏CRP(hs-CRP)采用免疫透射比浊法。采用高分辨超声技术测颈动脉内膜-中层厚度(IMT)及粥样硬化斑块。计算体质量指数(BMI)[BMI=体质量(kg)/身高(m)2]和肾小球滤过率(GFR)。
结果:1.慢性肾脏病患者的血清瘦素水平(14.86±5.92 ng/L)明显高于健康对照组(8.72±2.35ng/m1)p<0.01,且随肾功能恶化逐渐升高(CKD2~3期:12.0±2.56ng/ml;CKD4期:14.98±5.69ng/ml;CKD5期:19.78±5.23ng/ml)。慢性肾脏病患者的血清C-反应蛋白水平(2.65±1.32mg/L)明显高于健康对照组(1.52±0.88mg/L) p<0.01,且随肾功能恶化逐渐升高(CKD2~3期:1.85±0.86mg/L;CKD4期:2.96±0.99mg/L;CKD5期:3.55±1.26 mg/L);2.慢性肾脏病患者的颈动脉IMT水平(0.953±0.256mm)明显高于健康对照组(0.675±0.249mm)p<0.01,且随肾功能恶化逐渐升高(CKD2~3期:0.681±0.172mm;CKD4期:0.814±0.173mm;CKD5期:0.932±0.156mm);3.慢性肾脏病患者颈动脉超声异常组(IMT增厚:颈总动脉IMT≥0.9mm,或分叉处IMT>0.9mm;粥样斑块:突向管腔的局灶性动脉壁增厚,其厚度超过相邻区域IMT至少50%)血清瘦素水平(17.06±1.06ng/ml)和CRP水平(3.32±0.19mg/L)较颈动脉正常组血清瘦素水平(14.27±0.70ng/ml)和CRP(2.55±0.17mg/L)明显升高;4.慢性肾脏病患者高CRP组血清瘦素水平(18.78±5.52ng/ml)和颈动脉IMT(0.79±0.19mm)较CRP正常组血清瘦素水平(14.20±5.17ng/ml)和颈动脉IMT(0.70±0.15mm)明显升高;5.慢性肾脏病患者高瘦素组血清CRP水平(3.66±0.21mg/L)和颈动脉IMT(0.79±0.133mm)较低瘦素组血清CRP水平(2.24g±0.14mg/L)和颈动脉(0.71±0.054mm)明显升高(P<0.05);6.慢性肾脏病患者存在营养不良者(ALB<35g/L)血清瘦素水平(16.67±0.93ng/ml)、血清C-反应蛋白浓度(3.14±0.21mg/L)和颈动脉IMT(0.760±0.273 mm)较ALB≥35g/L组血清瘦素水平(14.17±0.75ng/ml)、血清C-反应蛋白浓度(2.49±0.19mg/L)和颈动脉IMT(0.716±0.273mm)明显升高;7.慢性肾脏病患者的血清瘦素水平与临床各项指标的直线相关分析显示:①血清瘦素与尿素氮、肌酐、C-反应蛋白、体重指数之间呈显著正相关(r=0.293,P<0.01;r=0.324,P<0.01;r=0.539,P<0.01;r=0.312,P<0.05);②血清瘦素与肾小球滤过率、血红蛋白、ALB之间呈明显负相关(r=-0.389,P<0.01;r=-0.454,P<0.01;r=-0.246, P<0.05),与年龄、Chol、TG无明显相关性(r=0.014, P>0.05;r=0.051, P>0.05;r=-0.055, P>0.05);8.多元线性回归分析显示:CKD患者颈动脉IMT与血清瘦素、C-反应蛋白、甘油三脂、血红蛋白密切相关(β=0.546,P<0.01;β=0.386,P<0.05;β=0.791,P<0.05;β=0.532,P<0.01),提示血浆瘦素与C-反应蛋白直接参与了动脉粥样硬化、粥样斑块的形成;9. Logistic逐步回归分析显示:瘦素(β=1.527,95%CI:1.028~1.438,P<0.05)是CKD患者并发动脉粥样硬化的独立危险因素之一。
结论:①慢性肾脏病患者存在高瘦素血症和微炎症状态,②高瘦素血症与微炎症状态和慢性肾脏病患者高发动脉粥样硬化性心血管事件相关;③血清瘦素可能微炎症反应相互作用而参与了慢性肾脏病患者动脉粥样硬化的形成。
Objective : 1.To investigate the changes of the concentration of serum leptin and C-reaction protein (CRP) with chronic kidney disease (CKD);2.To investigate the changes of the level of IMT of carotid artery with chronic kidney disease(CKD);3.To investigate the relationship between the level of the serum leptin , C-reaction protein (CRP) and each of the parameter for clinic with chronic kidney disease (CKD);4.To explore the relationship among the serum leptin, C-reaction protein (CRP) and chronic kidney disease (CKD),and the possible mechanism of leptin to atherosclerosis seen in chronic kidney disease (CKD).
Methods:We collected 79 patients with chronic kidney disease (51 males and 28 females) aged 44.22±13.47 (mean±SD). The standard of diagnosis by using K/DOQI guideline[1]. The primary diseases: 53 patients were chronic glomerulo- nephritis, 5 patients were hypertention nephritis, 3 patients were polycystic kidney,4 patients were obstructive nephropathy and 12 patients were etiology unknown. 79 patients with chronic kidney disease were classified into three groups according to glomerular filtration rate (GFR): (1) CKD2~3 stage groups included 26 patients (GFR30~90ml/min /1.73m2), (18 males and 8 females),the average age is 44.69±14.13 years; (2) CKD4 stage groups included 22 patients (GFR15~30ml/min/1.73m2), (16 males and 6 females),the average age is 42.7±12.63 years;(3) CKD 5stage groups included 31 patients (GFR<15ml/min /1.73m2), (17 males and 14 females),the average age is 45.19±13.78 years;(4) Healthy control group included 13 healthy volunteers (8 males and 5 females), aged 40.07±18.51 (mean±SD). Excluding standards:①Those who were infected, operated on and had trauma in recently one month;②To have acute cardiovascular disease (CVD) in recently one month;③Those who have used the cortical hormone or other immunity conditioner in recently six months ;④To affiliate malignancy, pregnancy;⑤diabetic nephropathy;⑥To have dialysis or renal transplantation. All the patients starved for 12 hours and the vein blood 6ml was sampled in the morning. The blood samples were tested by the automatic biochemical machine to measure the blood routine, blood creatinine, urea nitrogen, blood sugar, the cholesterol, triglyceride, high dense lipoprotein cholesterol, low dense lipoprotein, very low density lipoproteintotal protein, albumin. At the same time, the serum was centrifugally separated and saved in -70℃refrigerator to measure the leptin and CRP, The leptin was tested by the radio-immunity method and the reagents were provided by the Beijing Puer Weiye Biotechnical Institute. The CRP was tested by the rate-scatter turbidimetry method and the antiserum was provided by Shanghai Sun Biotechnical Institute. Seventy nine CKD patients and 13 healthy volunteers were involved in the study. The serum leptin was tested by the radio-immunity method;The CRP was tested by the rate-scatter turbidimetry method. Intima-medial thickness (IMT) of extracranial common carotid artery and the presence of atherosclerotic plaques were determined by using noninvasive high-resolution B-mode ultrasonography. To calculate body mass index (BMI) and glomerular filtration rate (GFR).
Results:1. Levels of leptin in the chronic kidney disease (CKD) patients were significantly higher than those in the healthy groups, and to elevate along with the deteriorate of kidney function;Levels of CRP in the chronic kidney disease (CKD) patients were significantly higher than those in the healthy groups, and to elevate along with the deterioration of kidney function;2. The IMT in carotid artery were significantly higher in CKD patients compared with the healthy groups, and to elevate along with the deteriorate of kidney function;3. It was found that patients with chronic kidney disease in the high IMT of carotid artery groups had serum CRP and serum leptin concentrations significantly increased compared with the normal IMT of carotid artery groups;4. It was found that patients with chronic kidney disease in the high CRP groups had serum leptin concentrations and IMT of carotid artery significantly increased compared with the normal CRP groups;5. It was found that patients with chronic kidney disease in hyperleptin groups had serum CRP concentrations and IMT of carotid artery significantly increased compared with the lowleptin groups; 6. It was found that patients with chronic kidney disease in the Alb <35g/L groups had serum CRP concentrations and IMT of carotid artery significantly increased compared with the Alb >35g/L groups;7. The linear correlations were found between the leptin and parameters in patients with chronic kidney disease (CKD) as follows:①The serum leptin levels were correlated positively with urea nitrogen serum creatinine C-reaction body mass index (BMI) (r=0.293,P<0.01;r=0.324,P<0.01;r=0.539,P<0.01;r=0.312,P<0.05);②The serum leptin levels were correlated negatively with glomerular filtration rate hemoglobin albumin (r=-0.389,P<0.01;r=-0.454,P<0.01;r=-0.246, P< 0.05),and were not correlated with age cholesterol triglyceride (r=0.014, P>0.05;r=0.051, P>0.05;r=-0.055, P>0.05) 8.The linear correlation regression analyses for IMT and serum leptin, serum CRP, TG, Hb, showed that serum leptin and serum CRP participated straightly in the atherosclerosis of vessel and the forming of atherosclerosis spot mass. 9. Logistic regression analysis further indicated that Leptin (β=1.527, 95%CI :1.028~1.438 , P<0.05) was an independent risk factor of atherosclerosis-related cardiovascular events in chronic disease (CKD).
Conclusions:①There is hyperleptin and micro inflamma- tory state in the chronic kidney disease (CKD) patients.②The leptin and microinflammatory state might be in close correlation with atherosclerosis-related cardiovascular events in chronic kidney disease (CKD).③The serum leptin and microinflamma- tion may result in accelerated atherosclerosis seen in chronic kidney disease (CKD).
引文
1 National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification and stratification. Am J Kidney Dis, 2002, 39(2 Suppl 1): S1-266
2 Foley RN, Parfrey PS, Sarnak MJ. Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis, 1998, 32(5 Suppl 3): S112-9
3 施蓓莉, 倪兆慧,周文彦,等.血浆不对称二甲基精氨酸与慢性肾脏及并非透析患者心血管并发症的关系.中华肾脏病杂志,2007, 23(6): 366-371
4 王丽,赵勇,曾和松,等.血清手素水平与冠状动脉病变程度的关系.临床心血管杂志,2006,22(12): 719-720
5 许竹梅, 赵水平. 超声检测AS的进展: 颈动脉内膜中层厚度的意义. 心血管病学进展, 1998, 19: 354-57
6 Sarnak MJ, Levey AS, Schoolwerth AC, et al. Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood PressureResearch, Clinical Cardiology, and Epidemiology and Prevention. Hypertension, 2003, 42(5): 1050-65
7 Qureshi AR, Alvestrand A, Divino-Filho JC, et al. Inflammation, malnutrition, and cardiac disease as predictors of mortality in hemodialysis patients. [J]. J Am Soc Nephrol, 2002, 13 Suppl 1: S28-36
8 侯凡凡.如何改善慢性肾脏病患者心血管疾病的预后. 中华内科杂志, 2002, 41: 507-508
9 Zhang Y, Proenca R, Maffei M, et al. Positional cloning of the mouse obses gene and its human homologue. Nature, 1994, 372(6505): 425-32
10 Merabet E, Dagogo-Jack S, Coyne DW, et al. Increased plasma leptin concentration in end-stage renal disease. J Clin Endocrinal Metab, 1997, 82(3): 847-50
11 Sharma K, Considine RV, Michael B, et al. Plasma leptin is partly cleared by the kidney and is elevated in hemodialysis patients. Kidney Int, 1997, 51(6): 1980-5
12 George A. The microinflammatory state in uremia: causes and potential consequences. J Am Soc Nephrol, 2001, 12(7):1549-57
13 陈江华, 何强, 徐莹. 维持性血液透析患者微炎症状态的认识与防治.[J]. 中华肾脏病杂志, 2005, 21(2): 117~18
14 戴慧莉, 钱家麒, 林爱武. 透析患者正性急性时相蛋白与血清白蛋白浓度关系的研究.[J]. 临床肾脏病杂志, 2003(3): 99-101
15 Zimmermann J, Herrlinger S, Pruy A, et al. Inflammation enhances cardiovascular risk and mortality in hemodialysis patients.[J]. Kidney Int, 1999, 55(2): 648-58
16 Stenvinkel P, Heinburger O, Paultre F. Strong association between malnutrition, inflammation, and atherosclerosis in chronic renal failure.[J]. Kidney Int, 1999, 55(5): 1899-911
17 Mehrotra R, Kopple JD. Nutritional management of maintenance dialysis patients: why aren’t we doing better? Annu Rev Nutr, 2001, 21: 343-79
18 Caglar K, Hakim RM, lkizler TA. Approaches to the reversal of malnutrition, inflammation, and atherosclerosis in end-stage renal disease.[J]. NutrRev, 2002, 60(11): 378-87
19 Peter S.Inflammatory and atherosclerotic interactions in the depleted uremic patient.[J]. Blood Purif, 2001, 19(1): 53-61
20 Young GA, Woodrow G, Kendll US, et al. Increased plasma leptin/ fat retio in patiens with chronic renal failure: a cause of malnutrition? Nephrol Dial Transplant, 1997, 12(11): 2318-23
21 Menon V, Greene T, Wang X, et al. C-reactive protein and albumin as predictors of all cause and cardiovascular mortality in chronic kidney disease. [J]. Kidney Int, 2005, 68(2): 766-72
22 Cooper BA, Penne EL, Bartlett LH, et al. Protein malnutrition and hypoalbuminemia as predictors of vascular events and mortality in ESRD. [J]. Am J Kidney Dis, 2004, 43(1): 61-6
23 Auer J, Berent R, Lassnig E, et al. C-reactive protein and coronary artery disease. [J]. Jpn Heart J, 2002, 43(6): 607-19
24 Ridker PM, Rifai N, Rose L, et al. Comparison of C-reactive protein and low-density lipoprotein cholesterol level in the prediction of first cardiovascular events. [J]. N Engl J Med, 2002, 347(20): 1557-65
25 Engstrom G, Lind P, Hedblad B, et al. Effects of cholesterol and inflammation sensitive plasma proteins on incidence of myocardial infarction and stroke in men. [J]. Circulation, 2002, 105(22): 2632-7
26 Sezer S, Ozdemir FN, Arat Z, et al. Triad of malnutrition, inflammation, and atherosclerosis in hemodialysis patient. [J]. Nephron, 2002, 91(3): 456-62
27 Arici M, Walls J. End-stage renal disease, atherosclerosis, and cardiovascular mortality: is C-reactive protein the missing link ? [J].Kidney Int, 2001, 59(2): 407-14
28 Otero M, Lago R, Lago F, et al. Leptin from fat to inflammation: old questions and new insights. [J]. FEBS Lett, 2005, 579(2): 295-301
29 Wouters EF. Local and Systemic Inflammation in Chronic Obstructive Pulmonary Disease. [J]. Proc Am Thorac Soc, 2005, 2(1): 26-33
30 Kato A, Odamaki M, Maruyama Y, et al. Association between circulating leptin and soluble receptors for tumor necrosis factor-alpha in hemodialysis patiens. Clin Nephrol. 2001, 56(5): 370-7
31 Maachi M, Pieroni L, Bruckert E, et al. Systemic low-grade inflammation is related to both circulating and adipose tissue TNF alpha, leptin and IL-6 levels in obese women. International Journal of Obesity, 2004, 28(8): 993-7
32 Pereira B, Poutsiaka D, King A, et al. In vitro production of interleukin-1 receptor antagonist in chronic renal failure, CAPD and HD. Kidney Int, 1992; 42(6): 1419-24
33 Bodary PF, Gu S, Shen Y, et al. Recombinant leptin promotes atherosclerosis and thromb in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol, 2005, 25(8): e119-22
34 Al-Hazimi AM, Syiamic AY. Relationship between plasma angiotensinII, leptin and arterial blood pressure[J]. Saudi Med J, 2004, 25(9): 1193-1198
35 Iwashita S, Tanida M, Terui N, et al. Direct measurement of renal sympathetic nervous activity in high fat diet-related hypertensive rats. [J]. Life Sci, 2002, 71(5): 537-46
36 Ciccone M,Vettor R, Pannacciulli N,et al. Plasma leptin is independently associated with the intima-media thickness of the common carotid artery. Int J Obes Relat Metab Disord,2001, 25(6): 805-10
37 Tritos NA, Manning WJ, Dania PG. Role of leptin in the development of cardiac hypertrophy in experimental animals and humans.[J]. Circulation, 2004, 109(7): e67
38 Wallace AM, McMahon AD, Packard CJ, et al. Plasma leptin and the risk of cardiovascular disease in the west of Scotland coronary prevention study (WOSCOPS). Circulation, 2001, 104(25): 3052-6
1 Zhang Y, Proenca R, Maffei M, et al. Positional cloning of the mouse obese gene and its human homonlogue. Nature, 1994, 372(6505): 425-32
2 Houseknecht KL, Portocarrero CP. Leptin and its receptors: regulators of whole-body energy homeostasis. [J]. Domest Anim Endocrinol, 1998, 15(6):457-75
3 Maedler K, Sergeev P, Ehses JA, et al. Leptin modulates beta cell expression of IL-1 receptor antagonist and release of IL-1beta in human islets. [J]. Proc Natl Acad Sci USA, 2004, 101(21): 8138-43
4 Okuya S, Tanabe K, Tanizawa Y, et al. Leptin increases the viability isolated rat pancreatic islets by suppressing apoptosis. [J]. Endocrinology, 2001, 142(11): 4827-30
5 Zarkesh-Esfaharli H, Pockley G, Metcalfe RA, et al. Hightdose leptin activates human leukocytes via receptor expression on monocytes. [J]. J Immunol, 2001, 167(8): 4593-9
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9 Sánchez-Pozo C, Rodriguez-Ba?o J, Domínguez-Castellano A, et al. leptin stimulate the oxidative burst in control monocytes but attenuates the oxidative burst in moncytes from HIV-infected patients. [J]. Clin Exp Immunol, 2003, 134(3): 464-69
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11 Caro JF, Sinha MK, Kolaczynski JW, et al. Leptin: the tale of an obesity gene. Diabetes, 1996, 45(11): 1455-62
12 Sharma K, Considine RV, Michael B, et al. Plasma leptin is partly cleared by the kidney and is elevated in hemodialysis patients. [J]. Kidney Int, 1997, 51(6): 1980-85
13. Meyer C, Robson D, Rackovsky N, et al. Role of the kidney in human leptin metabolism. [J]. Am J Physiol, 1997, 273(5 Pt 1): E903-7
14 Cumin F, Baum HP, Levens N. Mechanism of leptin removal from the circulation by the kidney. [J]. J Endocrinol 1997, 155(3): 577-85
15 Caglar K, Hakim RM, Ikizler TA,Approaches to the reversal of malnutrition, inflammation, and atherosclerosis in end-stage renal disease. [J]. Nutr Rev, 2002, 60(11): 378-87
16 Peter S. Inflammatory and atherosclerotic interactions in thedepleted uremic patient.[J]. Blood Purif, 2001, 19(1): 53-61
17 仇新霞,郑法雷,李艳.慢性肾衰患者贫血与血清瘦素的关系. 徐州医学院学报, 2003, 23(5): 424-27
18 Young GA, Woodrow G, Kendall S, et al. Increased plasma leptin/fat retio in patiens with chronic renal failure: a cause of malnutrition? Nephrol Dial Transplant, 1997, 12(11): 2318-23
19 陈秀益, 刘必成, 尹莲芳. 微炎症反应状态与终末期肾病. [J]. 临床荟萃, 2005, 20(12): 712-715
20 Otero M, Lago R, Lago F, et al. Leptin, from fat to inflammation: old questions and new insights. [J]. FEBS Lett, 2005, 579(2): 295-301
21 Wouters EF. Local and Systemic inflammation in Chronic Obstructive Pulmonary disease. [J]. Proc Am Thorac Soc, 2005, 2(1): 26-33
22 Kato A, Odamaki M, Maruyama Y, et al. Association between circulating leptin and soluble receptors for tumor necrosis factor-alpha in hemodialysis patiens, Clin Nephrol. 2001, 56(5); 370-7
23 Maachi M, Pieroni L, Bruckert E, et al.Systemic low-grade inflammation is related to both circulating and adipose tissue adipose tissue TNF-alpha,leptin and IL-6 levels in obese women. International Journal of Obesity, 2004, 28(8): 993-7
24 张义雄,俞雷,朱春玲等.P-选择素、瘦素与血液透析患者微炎症反应状态的关系及意义. [J]. 中国血液净化,2006, 5(1): 53-55
25 Pereira B, Poutsiaka D, King A, et al. In vitro production of interleukin-1 receptor antagonist in chronic renal failure, CAPD and HD. Kidney Int, 1992; 42(6): 1419-24
26 Cumin F, Baum HP, Levens N. Leptin is cleared from the circulation primarily by the kidney. Int J Obesity. 1996, 20(12): 1120-6
27 Dagego-Jack S, Ovalle F, Gearing B, et al. Hyperleptinemia in patients with end-stage renal disease undergoing continuous amlulatory peritoneal dialysis. Perit Dial Int, 1998, 18(1): 34-40
28 Kolaczynski JW, Nyce MR, Considine RV, et al. Acute and chronic effect of insulin on leptin production in humans: studies in vivo and in vitro. Diabetes, 1996, 45(5): 699-701
29 Wiesholzer M, Harm F, Hauser AC, et al. Inappropriately high plasma leptin levels in obese haemodialysis patients can be reduced by high flux haemodialysis and haemodiafiltration. [J]. Clin Sci(Colch), 1998, 94(4): 431-5
30 Coyne DW, Dagogo-Jack S, Klein S, et al. High-flux dialysis lowers plasma leptin concentration in chronic dialysis patients. [J]. Am J Kidney Dis, 1998, 32(6): 1031-5
31 龙泉,陈靖,顾勇.瘦素与肾脏. [J]. 2007, 30(3): 217-20
32 Kokot F, Adamczak M, Wiecek A;cek A, et al. Plasma immunoreactive leptin and neuropeptide Y levels in kidney transplant patients. [J]. Am J Nephrol, 1999, 19(1): 28-33
33 屈会起.瘦素与肾脏.[J]. 国外医学内科分册, 2000, 27(3): 111-14
34 Fruenhwald-Schultes B, Kern W, Bever J, et al. Elevated serum leptin concentrations in type 2 diabetic patients with microalbuminuria and macroalbuminuria. [J]. Metabolism. 1999, 48(10): 1290-3
35 李芳萍,陈黎红,程桦,等.血清瘦素水平与胰岛β细胞功能、胰岛素抵抗的关系. 新医学. 2003, 34(2): 74
36 Corsonello A, Perticone F, Malara A, et al. Leptin-dependent platelet aggregation in healthy, overweight and obese subjects. [J]. Int J Obes Relat Metab Disord, 2003, 27(5): 566-73
37 Bouloumie A, Marumo T, Lafontan M, et al. Leptin induces oxidative stress in human endothelial cells. [J]. FASEB J, 1999, 13(10): 1231-8
38 Verroti A, Bascizni F, De Simone M, et al. Serum leptin chances during weight loss in obese diabetic subjects with and without microalbuminuria. [J]. Diabetes Nutr Metab, 2001, 14(5): 283-7
39 Al-Hazimi AM, Syiamic AY. Relationship between plasma angiotensinII , leptin and arterial blood pressure. [J]. Saudi Med J, 2004, 25(9): 1193-8
40 Iwashita S, Tanida M, Terui N, et al. Direct measurement of renal sympathetic nervous activity in high-fat diet-related hypertensive rats. [J]. Life Sci, 2002, 71(5): 537-46
41 Loffreda S, Yang SQ, Lin HZ, et al. Leptin regulates proinflammatory immune responses. [J]. Faseb J, 1998, 12(1): 57-65
42 Park HY, Kwon HM, Lim HJ, et al. Potential role of leptin in angiogenesis: leptin induces endothelial cell proliferation and expression of matrix metalloproteinases in vivo and in vitro. [J]. Exp Mol Med, 2001, 33(2): 95-102
43 Oda A, Taniguchi T, Yokoyama M. Leptin stimulates rat aortic smooth muscle cell proliferation and migration. [J]. Kobe J Med Sci, 2001, 47(3): 141-50
44 黎明, 吴从愿, 詹志伟, 等. 血清瘦素水平与原发性高血压的相关性研究. [J]. 中华医学杂志, 2003, 83(12): 1058-61
45 Wolk R, Berger P, Lennon RJ, et al. Plasma leptin and prognosis in patients with established coronary atherosclerosis. [J]. J Am Coll Cardiol, 2004, 44(9): 1819-24
2 Foley RN, Parfrey PS, Sarnak MJ. Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis, 1998, 32(5 Suppl 3): S112-9
3 施蓓莉, 倪兆慧,周文彦,等.血浆不对称二甲基精氨酸与慢性肾脏及并非透析患者心血管并发症的关系.中华肾脏病杂志,2007, 23(6): 366-371
4 王丽,赵勇,曾和松,等.血清手素水平与冠状动脉病变程度的关系.临床心血管杂志,2006,22(12): 719-720
5 许竹梅, 赵水平. 超声检测AS的进展: 颈动脉内膜中层厚度的意义. 心血管病学进展, 1998, 19: 354-57
6 Sarnak MJ, Levey AS, Schoolwerth AC, et al. Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood PressureResearch, Clinical Cardiology, and Epidemiology and Prevention. Hypertension, 2003, 42(5): 1050-65
7 Qureshi AR, Alvestrand A, Divino-Filho JC, et al. Inflammation, malnutrition, and cardiac disease as predictors of mortality in hemodialysis patients. [J]. J Am Soc Nephrol, 2002, 13 Suppl 1: S28-36
8 侯凡凡.如何改善慢性肾脏病患者心血管疾病的预后. 中华内科杂志, 2002, 41: 507-508
9 Zhang Y, Proenca R, Maffei M, et al. Positional cloning of the mouse obses gene and its human homologue. Nature, 1994, 372(6505): 425-32
10 Merabet E, Dagogo-Jack S, Coyne DW, et al. Increased plasma leptin concentration in end-stage renal disease. J Clin Endocrinal Metab, 1997, 82(3): 847-50
11 Sharma K, Considine RV, Michael B, et al. Plasma leptin is partly cleared by the kidney and is elevated in hemodialysis patients. Kidney Int, 1997, 51(6): 1980-5
12 George A. The microinflammatory state in uremia: causes and potential consequences. J Am Soc Nephrol, 2001, 12(7):1549-57
13 陈江华, 何强, 徐莹. 维持性血液透析患者微炎症状态的认识与防治.[J]. 中华肾脏病杂志, 2005, 21(2): 117~18
14 戴慧莉, 钱家麒, 林爱武. 透析患者正性急性时相蛋白与血清白蛋白浓度关系的研究.[J]. 临床肾脏病杂志, 2003(3): 99-101
15 Zimmermann J, Herrlinger S, Pruy A, et al. Inflammation enhances cardiovascular risk and mortality in hemodialysis patients.[J]. Kidney Int, 1999, 55(2): 648-58
16 Stenvinkel P, Heinburger O, Paultre F. Strong association between malnutrition, inflammation, and atherosclerosis in chronic renal failure.[J]. Kidney Int, 1999, 55(5): 1899-911
17 Mehrotra R, Kopple JD. Nutritional management of maintenance dialysis patients: why aren’t we doing better? Annu Rev Nutr, 2001, 21: 343-79
18 Caglar K, Hakim RM, lkizler TA. Approaches to the reversal of malnutrition, inflammation, and atherosclerosis in end-stage renal disease.[J]. NutrRev, 2002, 60(11): 378-87
19 Peter S.Inflammatory and atherosclerotic interactions in the depleted uremic patient.[J]. Blood Purif, 2001, 19(1): 53-61
20 Young GA, Woodrow G, Kendll US, et al. Increased plasma leptin/ fat retio in patiens with chronic renal failure: a cause of malnutrition? Nephrol Dial Transplant, 1997, 12(11): 2318-23
21 Menon V, Greene T, Wang X, et al. C-reactive protein and albumin as predictors of all cause and cardiovascular mortality in chronic kidney disease. [J]. Kidney Int, 2005, 68(2): 766-72
22 Cooper BA, Penne EL, Bartlett LH, et al. Protein malnutrition and hypoalbuminemia as predictors of vascular events and mortality in ESRD. [J]. Am J Kidney Dis, 2004, 43(1): 61-6
23 Auer J, Berent R, Lassnig E, et al. C-reactive protein and coronary artery disease. [J]. Jpn Heart J, 2002, 43(6): 607-19
24 Ridker PM, Rifai N, Rose L, et al. Comparison of C-reactive protein and low-density lipoprotein cholesterol level in the prediction of first cardiovascular events. [J]. N Engl J Med, 2002, 347(20): 1557-65
25 Engstrom G, Lind P, Hedblad B, et al. Effects of cholesterol and inflammation sensitive plasma proteins on incidence of myocardial infarction and stroke in men. [J]. Circulation, 2002, 105(22): 2632-7
26 Sezer S, Ozdemir FN, Arat Z, et al. Triad of malnutrition, inflammation, and atherosclerosis in hemodialysis patient. [J]. Nephron, 2002, 91(3): 456-62
27 Arici M, Walls J. End-stage renal disease, atherosclerosis, and cardiovascular mortality: is C-reactive protein the missing link ? [J].Kidney Int, 2001, 59(2): 407-14
28 Otero M, Lago R, Lago F, et al. Leptin from fat to inflammation: old questions and new insights. [J]. FEBS Lett, 2005, 579(2): 295-301
29 Wouters EF. Local and Systemic Inflammation in Chronic Obstructive Pulmonary Disease. [J]. Proc Am Thorac Soc, 2005, 2(1): 26-33
30 Kato A, Odamaki M, Maruyama Y, et al. Association between circulating leptin and soluble receptors for tumor necrosis factor-alpha in hemodialysis patiens. Clin Nephrol. 2001, 56(5): 370-7
31 Maachi M, Pieroni L, Bruckert E, et al. Systemic low-grade inflammation is related to both circulating and adipose tissue TNF alpha, leptin and IL-6 levels in obese women. International Journal of Obesity, 2004, 28(8): 993-7
32 Pereira B, Poutsiaka D, King A, et al. In vitro production of interleukin-1 receptor antagonist in chronic renal failure, CAPD and HD. Kidney Int, 1992; 42(6): 1419-24
33 Bodary PF, Gu S, Shen Y, et al. Recombinant leptin promotes atherosclerosis and thromb in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol, 2005, 25(8): e119-22
34 Al-Hazimi AM, Syiamic AY. Relationship between plasma angiotensinII, leptin and arterial blood pressure[J]. Saudi Med J, 2004, 25(9): 1193-1198
35 Iwashita S, Tanida M, Terui N, et al. Direct measurement of renal sympathetic nervous activity in high fat diet-related hypertensive rats. [J]. Life Sci, 2002, 71(5): 537-46
36 Ciccone M,Vettor R, Pannacciulli N,et al. Plasma leptin is independently associated with the intima-media thickness of the common carotid artery. Int J Obes Relat Metab Disord,2001, 25(6): 805-10
37 Tritos NA, Manning WJ, Dania PG. Role of leptin in the development of cardiac hypertrophy in experimental animals and humans.[J]. Circulation, 2004, 109(7): e67
38 Wallace AM, McMahon AD, Packard CJ, et al. Plasma leptin and the risk of cardiovascular disease in the west of Scotland coronary prevention study (WOSCOPS). Circulation, 2001, 104(25): 3052-6
1 Zhang Y, Proenca R, Maffei M, et al. Positional cloning of the mouse obese gene and its human homonlogue. Nature, 1994, 372(6505): 425-32
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