腹膜透析病人营养不良与心血管疾病的关系
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摘要
目的探讨持续性非卧床腹膜透析(continuous ambulatory peritoneal dialysis，CAPD)患者细胞外液(extracellular water，ECW)与总体水(total body water，TBW)的比率(E／T)与脉搏波速度(pulse wave velocity，PWV)的关系。方法选取同一中心56名情况稳定的CAPD病人为研究对象。应用自动PWV分析仪测定颈动脉—股动脉脉搏波速度。应用多频生物电阻抗分析仪对患者的容量状态进行评估，得出E／T值。同时应用标准测量法进行相应生化检查。对相应指标进行相关及多元回归分析以判断相应指标之间的关系，筛选PWV的影响因素。结果Pearson相关分析显示PWV与E／T(r=0.454，P=0.001)，细胞外液与细胞内液之比(extracellular water／intracellular water，E／I)(r=0.456，P=0.001)，脉压(r=0.649，P＜0.001)，年龄(r=0.404，P=0.002)，血清白蛋白(r=-0.346，P=0.01)，C-反应蛋白(C-reactive protein，CRP)(r=0.327，P=0.025)显著相关。多元线性逐步回归结果显示E／T(β=0.472，P=0.001)、脉压(β=0.442，P=0.001)、CRP(β=0.246，P=0.05)是PWV增加的独立危险因素。三者一起决定了PWV变化的58.1％。其中仅E／T就决定了PWV变化的37.8％。回归方程：Y=-7.064+29.04X_1+0.051X_2+0.077X_3(X_1=E／T，X_2=PP，X_3=CRP)。结论CAPD病人中E／T增加与PWV的增大密切相关。E／T同脉压、CRP一起是CAPD病人PWV增大的独立危险因素，这提示在透析病人中容量超负荷可能是通过动脉硬化程度的加重导致心血管疾病发生率和死亡率增加的。
目的低白蛋白血症是透析病人心血管疾病发病率及死亡率的一个重要危险因子，但其内在机制尚不明确。本研究以一组持续非卧床腹膜透析(continuous ambulatory peritoneal dialysis，CAPD)病人为研究对象，揭示血清白蛋白与大动脉僵硬度的金指标——脉搏波传播速度(pulse wave velocity，PWV)之间的关系。方法选取同一腹透中心62名临床情况稳定的CAPD病人为研究对象。其中男性病人为43.5％。他们的平均年龄为63±12岁，平均透析龄为23±22月。标准法测量血清白蛋白浓度、C—反应蛋白(C-reactive protein，CRP)及PWV等。应用相关和逐步多元回归分析PWV的影响因素。结果结果显示，PWV与血清白蛋白浓度(r=-0.357，P＜0.01)呈负相关，与年龄(r=0.35，P＜0.01)、糖尿病状态(是=1，否=0；r=0.292，P＜0.05)、收缩压(r=0.493，P＜0.001)、CRP浓度(r=0.295，P＜0.05)呈正相关。多元逐步回归分析发现收缩压(β=0.615，P＜0.001)、年龄(β=0.414，P＜0.01)、血清白蛋白浓度(β=0.315，P＜0.05)及总胆固醇浓度(β=0.275，P＜0.05)是PWV的独立影响因子。(决定系数=0.627)。结论在CAPD病人中，低白蛋白血症可能是通过大动脉僵硬度的增加导致心血管事件发病率和死亡率增加的。
目的验证低蛋白血症和心血管疾病发生之间是通过动脉硬化程度的加重来实现的这一假想。方法该研究以184个(83男／101女)持续性非卧床腹膜透析(continuous ambulatory peritoneal dialysis，CAPD)病人为研究对象。测定病人的血清白蛋白等生化指标，并测量肱动脉血压，进而计算出脉压。对该组病人进行相关及多元回归分析，以判断低白蛋白血症与脉压的关系。根据病人的血清白蛋白水平将病人分为两组：低白蛋白血症组(＜35g／L)及正常白蛋白组(≥35g／L)。将两组病人在年龄、性别、糖尿病比例、血脂水平及抗高血压药物等方面进行匹配，剩余132个病人，其中低白蛋白血症组60人，正常蛋白组72人，观察两组病人的脉压的不同。结果低白蛋白血症组病人的脉压要明显高于正常白蛋白组病人的脉压(67±17 mmHg vs．55±17mmHg，P＜0.01)。血清白蛋白水平分别与收缩压(r=-0.211，P＜0.01)及脉压(r=-0.281，P＜0.001)呈负相关。多元回归分析显示脉压受年龄(β=0.451，P＜0.05)，体重指数(β=1.703，P＜0.05)及血清白蛋白(β=-2.492，P＜0.01)影响。结论在CAPD病人中，低白蛋白血症与脉压升高密切相关。血清白蛋白水平和年龄、体重指数是脉压增高的独立危险因素，这提示低白蛋白血症可能是通过动脉硬化程度的加重使心血管疾病发病率及死亡率升高的。
目的探讨持续性非卧床腹膜透析(continuous ambulatory peritoneal dialysis，CAPD)患者细胞外液(extracellular water，ECW)与总体水(total body water，TBW)的比率(E／T)与脉压的关系。方法选取同一中心74名情况稳定的CAPD病人为研究对象。测量肱动脉血压得出脉压。应用多频生物电阻抗分析仪对患者的容量状态进行评估，得出E／T值。同时应用标准测量法进行相应生化检查。对相应指标进行相关及多元回归分析以判断相应指标之间的关系，筛选脉压的影响因素。结果Pearson相关分析显示脉压与E／T(r=0.691，P＜0.001)，细胞外液与细胞内液之比(extracellular water／intracellular water，E／I)(r=0.695，P＜0.001)，收缩压(r=0.78，P＜0.001)，舒张压(r=-0.402，P＜0.001)，年龄(r=0.427，P＜0.001)，血清白蛋白(r=-0.36，P=0.002)，C-反应蛋白(C-reactive protein，CRP)(r=0.367，P=0.008)及糖尿病状态(r=0.25，P=0.031)显著相关。多元线性逐步回归结果显示E／T(β=0.67，P＜0.001)和CRP(β=0.253，P=0.016)是脉压增加的独立危险因素。二者一起决定了脉压变化的55.7％。其中仅E／T就决定了脉压变化的50.4％。回归方程：Y=-111.81+326.361X_1+0.584X_2(Y=PP；X_1=E／T；X_2=CRP)结论CAPD病人中E／T增加与脉压的增大密切相关。E／T同CRP一起是CAPD病人脉压增大的独立危险因素，这提示在透析病人中容量超负荷可能是通过动脉硬化程度的加重导致心血管疾病发生率和死亡率增加的。
Objective To research the assosiation between E/T (extracellular water to-total body water ratio) and pulse wave velocity (PWV) in patients on continuous ambulatory peritoneal dialysis(CAPD). Methods Clinical stable CAPD patients (n=56, 26M/30F) in a single center were included. Carotid-femoral PWV was measured with a validated automatic device and was used as an index of large arterial stiffness. Multiple-frequency bioelectrical impedance analysis was used to record the values for ECW, intracellular water (ICW), and total-body water. Based on these data, E/T also was calculated. In addition, some biochemical indices, such as serum albumin, blood urea nitrogen, serum creatinine, serum triglycerides, total cholesterol lipoprotein, low-density lipoprotein, high-density lipoprotein, alanine and aspartate transaminase etc were determined with standard methods. Pearson' s correlation and multiple regression analysis were performed to identify the relationship between E/T and PWV. Results PWV was strongly associated with E/T (r=0. 454, p=0. 001), E/I (r=0. 456, p=0. 001), pulse pressure (PP) ( r=0. 649 , p<0. 001), age (r=0. 404, p=0. 002), serum albumin (r=-0. 346, p=0. 01) and CRP (r=0. 327, p=0. 025) , respectively. Multiple regression analysis showed that PWV was independently determined by E/T (β=0.472, P =0. 001)、 PP(β=0. 442, P=0. 001) and CRP( β=0. 246, P=0. 05). They accounted for 58. 1% of the total variance and E/T alone reprensented 37. 8% of the explained variance. The regression equation: Y=-7. 064+29. 04X_1+0. 051X_2+0. 077X_3 (X_1 =E/T, X_2=PP, X_3=CRP) Conclusion E/T was closely associated with PWV in peritoneal dialysis patients. E/T, in addition to PP and CRP, was an independent risk factor for elevated PWV in CAPD patients, suggesting that increased arterial stiffness might be the link between fluid overload and cardiovascular events and mortality in dialysis patients. Objective Hypoalbuminemia has been shown as a risk factor for cardiovascular events and mortality in dialysis patients but the underlying mechanism remained inconclusive. The aim of the present study was to assess the association between serum albumin and pulse wave velocity (PWV)—the marker of arterial stiffness in a group of patients on continuous ambulatory peritoneal dialysis (CAPD). Methods Clinical stable CAPD patients (n=62) in a single center was included. Of the 62 patients studied, 43.5% were men. The average age was 63 ± 12 years and mean dialysis duration was 23±22 months. Serum albumin, C-reactive protein (CRP) and carotid-femoral PWV were measured. Results Of the 62 patients studied, 43. 5% were men. The mean serum albumin concentration of total subjects was 37±4g/L, and PWV was 11.9 ± 2.3m/s. PWV was positively correlated with age (r=0.35, P<0.01), diabetic status (yes=1, no=0; r=0.292, P <0.05), SBP (r =0. 493, P <0. 001) and CRP (r=0. 295, P <0. 05), but negatively correlated with serum albumin (r=-0.357, P<0.01). In stepwise multiple regression analysis, systolic blood pressure (β=0.615, P<0.001), age (β=0.414, P<0.01), serum albumin (β=-0.315, P<0.05) and total cholesterol (β=0.275, P<0.05) were independent determinants of PWV after adjusting gender, height, diabetic status, dialysis duration, diastolic blood pressure, antihypertensive medication, C-reactive protein, calcium concentration and total cholesterol (adjusted R square=0.627). Conclusion The independent association between serum albumin and pulse wave velocity suggested that increased arterial stiffness might be the link between hypoalbuminemia and increased cardiovascular events and mortality in dialysis patients. Objective To validate the hypothesis that the possible link between hypoalbuminemia and cardiovascular disease was arterial stiffness. Methods Clinical stable CAPD patients (n=184, 83M/101F) in a single center was included. Serum albumin, C-reactive protein (CRP) and brachial blood pressure were measured. Pearson's correlation and multiple regression analysis were performed to identify the relationship between hypoalbuminemia and PP. In addition, patients were divided into two groups according to the serum albumin concentration: hypoalbuminemia group (<35g/L) and normal-albumin group (≥35g/L). The two groups were matched in age, sex,diabetes,antihypertensive medication, serum lipid and so on,then 132 patients remained. There were 60 patients in hypoalbuminenia group and 72 in normal-albumin group. Results PP in hypoalbuminemia group was significantly higher than that in normal-albumin group (67±17 vs. 55±17 mmHg, P<0.01). Serum albumin was negatively associated with systolic blood pressure (r=-0.211, P<0.01) and PP (r=-0.281, P<0.001), respectively. Multiple regression analysis showed that PP was determined by age (odds ratio=0.451, P<0.05), body mass index (odds ratio=1.703, P<0.05) and serum albumin (odds ratio=-2.492, P<0.01). Conclusion Hypoalbuminemia was closely associated with increased pulse pressure in peritoneal dialysis patients. Serum albumin, in addition to age and body mass index, was an independent risk factor for elevated pulse pressure in CAPD patients, suggesting that increased arterial stiffness might be the link between hypoalbuminemia and cardiovascular events and mortality in dialysis patients. Objective To research the assosiation between E/T (extracellular water to-total body water ratio) and pulse pressure (PP) in patients on continuous ambulatory peritoneal dialysis (CAPD). Methods Clinical stable CAPD patients (n=74, 32M/42F) were included. Brachial blood pressure was measured twice in sitting position after patients had rested more than ten minutes. PP was calculated as systolic blood pressure (SBP) minus diastolic blood pressure (DBP) and it was used as an index of large arterial stiffness. Multiple-frequency bioelectrical impedance analysis was used to record the values for ECW, intracellular water (ICW), and total-body water. Based on these data, E/T also was calculated. In addition, some biochemical indices were determined with standard methods. Pearson' s correlation and multiple regression analysis were performed to identify the relationship between E/T and PP. Results PP was strongly associated with E/T(extracellular water/ total body water) (r=0.691, P <0.001) , E/I (extracellular water/intracellular water) (r=0.456,p=0.001),SBP (r=0.78, P<0.001) , DBP, (r =-0.402, P<0.001), age (r=0.427, P<0.001) , serum albumin (r=-0.36, P=0.002) , C-reactive protein( CRP) (r =0.367, P=0.008) and diabetes (r=0.25, P=0.031) , respectively. Multiple regression analysis showed that PP was independently determined by E/T ( β=0. 67, P<0.001) and CRP(β=0. 253, P =0.016). They accounted for 55.7% of the total variance and E/T alone reprensented 50.4% of the explained variance. The regression equation: Y=-111. 81+326.361X_1+0.584X_2(Y=PP;X_1=E/T;X_2= CRP) Conclusion E/T was closely associated with PP in peritoneal dialysis patients. E/T, in addition to CRP, was an independent risk factor for elevated PP in CAPD patients, suggesting that increased arterial stiffness might be the link between fluid overload and cardiovascular events and mortality in dialysis patients.
目的低白蛋白血症是透析病人心血管疾病发病率及死亡率的一个重要危险因子，但其内在机制尚不明确。本研究以一组持续非卧床腹膜透析(continuous ambulatory peritoneal dialysis，CAPD)病人为研究对象，揭示血清白蛋白与大动脉僵硬度的金指标——脉搏波传播速度(pulse wave velocity，PWV)之间的关系。方法选取同一腹透中心62名临床情况稳定的CAPD病人为研究对象。其中男性病人为43.5％。他们的平均年龄为63±12岁，平均透析龄为23±22月。标准法测量血清白蛋白浓度、C—反应蛋白(C-reactive protein，CRP)及PWV等。应用相关和逐步多元回归分析PWV的影响因素。结果结果显示，PWV与血清白蛋白浓度(r=-0.357，P＜0.01)呈负相关，与年龄(r=0.35，P＜0.01)、糖尿病状态(是=1，否=0；r=0.292，P＜0.05)、收缩压(r=0.493，P＜0.001)、CRP浓度(r=0.295，P＜0.05)呈正相关。多元逐步回归分析发现收缩压(β=0.615，P＜0.001)、年龄(β=0.414，P＜0.01)、血清白蛋白浓度(β=0.315，P＜0.05)及总胆固醇浓度(β=0.275，P＜0.05)是PWV的独立影响因子。(决定系数=0.627)。结论在CAPD病人中，低白蛋白血症可能是通过大动脉僵硬度的增加导致心血管事件发病率和死亡率增加的。
目的验证低蛋白血症和心血管疾病发生之间是通过动脉硬化程度的加重来实现的这一假想。方法该研究以184个(83男／101女)持续性非卧床腹膜透析(continuous ambulatory peritoneal dialysis，CAPD)病人为研究对象。测定病人的血清白蛋白等生化指标，并测量肱动脉血压，进而计算出脉压。对该组病人进行相关及多元回归分析，以判断低白蛋白血症与脉压的关系。根据病人的血清白蛋白水平将病人分为两组：低白蛋白血症组(＜35g／L)及正常白蛋白组(≥35g／L)。将两组病人在年龄、性别、糖尿病比例、血脂水平及抗高血压药物等方面进行匹配，剩余132个病人，其中低白蛋白血症组60人，正常蛋白组72人，观察两组病人的脉压的不同。结果低白蛋白血症组病人的脉压要明显高于正常白蛋白组病人的脉压(67±17 mmHg vs．55±17mmHg，P＜0.01)。血清白蛋白水平分别与收缩压(r=-0.211，P＜0.01)及脉压(r=-0.281，P＜0.001)呈负相关。多元回归分析显示脉压受年龄(β=0.451，P＜0.05)，体重指数(β=1.703，P＜0.05)及血清白蛋白(β=-2.492，P＜0.01)影响。结论在CAPD病人中，低白蛋白血症与脉压升高密切相关。血清白蛋白水平和年龄、体重指数是脉压增高的独立危险因素，这提示低白蛋白血症可能是通过动脉硬化程度的加重使心血管疾病发病率及死亡率升高的。
目的探讨持续性非卧床腹膜透析(continuous ambulatory peritoneal dialysis，CAPD)患者细胞外液(extracellular water，ECW)与总体水(total body water，TBW)的比率(E／T)与脉压的关系。方法选取同一中心74名情况稳定的CAPD病人为研究对象。测量肱动脉血压得出脉压。应用多频生物电阻抗分析仪对患者的容量状态进行评估，得出E／T值。同时应用标准测量法进行相应生化检查。对相应指标进行相关及多元回归分析以判断相应指标之间的关系，筛选脉压的影响因素。结果Pearson相关分析显示脉压与E／T(r=0.691，P＜0.001)，细胞外液与细胞内液之比(extracellular water／intracellular water，E／I)(r=0.695，P＜0.001)，收缩压(r=0.78，P＜0.001)，舒张压(r=-0.402，P＜0.001)，年龄(r=0.427，P＜0.001)，血清白蛋白(r=-0.36，P=0.002)，C-反应蛋白(C-reactive protein，CRP)(r=0.367，P=0.008)及糖尿病状态(r=0.25，P=0.031)显著相关。多元线性逐步回归结果显示E／T(β=0.67，P＜0.001)和CRP(β=0.253，P=0.016)是脉压增加的独立危险因素。二者一起决定了脉压变化的55.7％。其中仅E／T就决定了脉压变化的50.4％。回归方程：Y=-111.81+326.361X_1+0.584X_2(Y=PP；X_1=E／T；X_2=CRP)结论CAPD病人中E／T增加与脉压的增大密切相关。E／T同CRP一起是CAPD病人脉压增大的独立危险因素，这提示在透析病人中容量超负荷可能是通过动脉硬化程度的加重导致心血管疾病发生率和死亡率增加的。
Objective To research the assosiation between E/T (extracellular water to-total body water ratio) and pulse wave velocity (PWV) in patients on continuous ambulatory peritoneal dialysis(CAPD). Methods Clinical stable CAPD patients (n=56, 26M/30F) in a single center were included. Carotid-femoral PWV was measured with a validated automatic device and was used as an index of large arterial stiffness. Multiple-frequency bioelectrical impedance analysis was used to record the values for ECW, intracellular water (ICW), and total-body water. Based on these data, E/T also was calculated. In addition, some biochemical indices, such as serum albumin, blood urea nitrogen, serum creatinine, serum triglycerides, total cholesterol lipoprotein, low-density lipoprotein, high-density lipoprotein, alanine and aspartate transaminase etc were determined with standard methods. Pearson' s correlation and multiple regression analysis were performed to identify the relationship between E/T and PWV. Results PWV was strongly associated with E/T (r=0. 454, p=0. 001), E/I (r=0. 456, p=0. 001), pulse pressure (PP) ( r=0. 649 , p<0. 001), age (r=0. 404, p=0. 002), serum albumin (r=-0. 346, p=0. 01) and CRP (r=0. 327, p=0. 025) , respectively. Multiple regression analysis showed that PWV was independently determined by E/T (β=0.472, P =0. 001)、 PP(β=0. 442, P=0. 001) and CRP( β=0. 246, P=0. 05). They accounted for 58. 1% of the total variance and E/T alone reprensented 37. 8% of the explained variance. The regression equation: Y=-7. 064+29. 04X_1+0. 051X_2+0. 077X_3 (X_1 =E/T, X_2=PP, X_3=CRP) Conclusion E/T was closely associated with PWV in peritoneal dialysis patients. E/T, in addition to PP and CRP, was an independent risk factor for elevated PWV in CAPD patients, suggesting that increased arterial stiffness might be the link between fluid overload and cardiovascular events and mortality in dialysis patients. Objective Hypoalbuminemia has been shown as a risk factor for cardiovascular events and mortality in dialysis patients but the underlying mechanism remained inconclusive. The aim of the present study was to assess the association between serum albumin and pulse wave velocity (PWV)—the marker of arterial stiffness in a group of patients on continuous ambulatory peritoneal dialysis (CAPD). Methods Clinical stable CAPD patients (n=62) in a single center was included. Of the 62 patients studied, 43.5% were men. The average age was 63 ± 12 years and mean dialysis duration was 23±22 months. Serum albumin, C-reactive protein (CRP) and carotid-femoral PWV were measured. Results Of the 62 patients studied, 43. 5% were men. The mean serum albumin concentration of total subjects was 37±4g/L, and PWV was 11.9 ± 2.3m/s. PWV was positively correlated with age (r=0.35, P<0.01), diabetic status (yes=1, no=0; r=0.292, P <0.05), SBP (r =0. 493, P <0. 001) and CRP (r=0. 295, P <0. 05), but negatively correlated with serum albumin (r=-0.357, P<0.01). In stepwise multiple regression analysis, systolic blood pressure (β=0.615, P<0.001), age (β=0.414, P<0.01), serum albumin (β=-0.315, P<0.05) and total cholesterol (β=0.275, P<0.05) were independent determinants of PWV after adjusting gender, height, diabetic status, dialysis duration, diastolic blood pressure, antihypertensive medication, C-reactive protein, calcium concentration and total cholesterol (adjusted R square=0.627). Conclusion The independent association between serum albumin and pulse wave velocity suggested that increased arterial stiffness might be the link between hypoalbuminemia and increased cardiovascular events and mortality in dialysis patients. Objective To validate the hypothesis that the possible link between hypoalbuminemia and cardiovascular disease was arterial stiffness. Methods Clinical stable CAPD patients (n=184, 83M/101F) in a single center was included. Serum albumin, C-reactive protein (CRP) and brachial blood pressure were measured. Pearson's correlation and multiple regression analysis were performed to identify the relationship between hypoalbuminemia and PP. In addition, patients were divided into two groups according to the serum albumin concentration: hypoalbuminemia group (<35g/L) and normal-albumin group (≥35g/L). The two groups were matched in age, sex,diabetes,antihypertensive medication, serum lipid and so on,then 132 patients remained. There were 60 patients in hypoalbuminenia group and 72 in normal-albumin group. Results PP in hypoalbuminemia group was significantly higher than that in normal-albumin group (67±17 vs. 55±17 mmHg, P<0.01). Serum albumin was negatively associated with systolic blood pressure (r=-0.211, P<0.01) and PP (r=-0.281, P<0.001), respectively. Multiple regression analysis showed that PP was determined by age (odds ratio=0.451, P<0.05), body mass index (odds ratio=1.703, P<0.05) and serum albumin (odds ratio=-2.492, P<0.01). Conclusion Hypoalbuminemia was closely associated with increased pulse pressure in peritoneal dialysis patients. Serum albumin, in addition to age and body mass index, was an independent risk factor for elevated pulse pressure in CAPD patients, suggesting that increased arterial stiffness might be the link between hypoalbuminemia and cardiovascular events and mortality in dialysis patients. Objective To research the assosiation between E/T (extracellular water to-total body water ratio) and pulse pressure (PP) in patients on continuous ambulatory peritoneal dialysis (CAPD). Methods Clinical stable CAPD patients (n=74, 32M/42F) were included. Brachial blood pressure was measured twice in sitting position after patients had rested more than ten minutes. PP was calculated as systolic blood pressure (SBP) minus diastolic blood pressure (DBP) and it was used as an index of large arterial stiffness. Multiple-frequency bioelectrical impedance analysis was used to record the values for ECW, intracellular water (ICW), and total-body water. Based on these data, E/T also was calculated. In addition, some biochemical indices were determined with standard methods. Pearson' s correlation and multiple regression analysis were performed to identify the relationship between E/T and PP. Results PP was strongly associated with E/T(extracellular water/ total body water) (r=0.691, P <0.001) , E/I (extracellular water/intracellular water) (r=0.456,p=0.001),SBP (r=0.78, P<0.001) , DBP, (r =-0.402, P<0.001), age (r=0.427, P<0.001) , serum albumin (r=-0.36, P=0.002) , C-reactive protein( CRP) (r =0.367, P=0.008) and diabetes (r=0.25, P=0.031) , respectively. Multiple regression analysis showed that PP was independently determined by E/T ( β=0. 67, P<0.001) and CRP(β=0. 253, P =0.016). They accounted for 55.7% of the total variance and E/T alone reprensented 50.4% of the explained variance. The regression equation: Y=-111. 81+326.361X_1+0.584X_2(Y=PP;X_1=E/T;X_2= CRP) Conclusion E/T was closely associated with PP in peritoneal dialysis patients. E/T, in addition to CRP, was an independent risk factor for elevated PP in CAPD patients, suggesting that increased arterial stiffness might be the link between fluid overload and cardiovascular events and mortality in dialysis patients.
引文
1. CANADA-USA (CANUSA) Peritoneal Dialysis Study Group. Adequacy of dialysis and nutrition in continuous peritoneal dialysis:association with clinical outcome. J.Am.Soc.Nephrol. 1996;7:198-207.
2. Chung SH, Lindholm B, Lee HB. Influence of initial nutritional status on continuous ambulatory peritoneal dialysis patient survival. Perit.Dial.Int. 2000;20:19-26.
3. Bergstrom J, Lindholm B. Malnutrition, cardiac disease, and mortality: an integrated point of view. Am J.Kidney Dis. 1998;32:834-841.
4. Fung F, Sherrard DJ, Gillen DL et al. Increased risk for cardiovascular mortality among malnourished end-stage renal disease patients. Am J.Kidney Dis. 2002;40:307-314.
5. Cooper BA, Penne EL, Bartlett LH, Pollock CA. Protein malnutrition and hypoalbuminemia as predictors of vascular events and mortality in ESRD. AmJ.Kidney Dis. 2004;43:61-66.
6. Covic A, Gusbeth-Tatomir P, Goldsmith DJ. Arterial stiffness in renal patients: an update. Am J Kidney Dis 2005;45:965-977.
7. Asmar R, Rudnichi A, Blacher J, London GM, Safar ME. Pulse pressure and aortic pulse wave are markers of cardiovascular risk in hypertensive populations. Am J Hypertens. 2001;14:91-97.
8. Laurent S, Boutouyrie P, Asmar R et al. Aortic stiffness is an independent risk predictor of all-cause and mortality in hypertensive patients. Hypertension 2001;37:1236-1241.
9. Hansen TW, Staessen JA, Torp-Pedersen C et al. Prognostic value of aortic pulse wave velocity as index of arterial stiffness in the general population.Circulation 2006; 113:664-670.
10. Laurent S. Surrogate measures of arterial stiffness: do they have additive predictive value or are they only surrogates of a surrogate? Hypertension 2006;47:325-326.
11. O'Rourke MF, Staessen JA, Vlachojannis JA, Duprez D, Plante GE. Clinical application of arterial stiffness:definitions and reference values. Am J Hypertens. 2002; 15:426-444.
12. Combe C, McCullough KP, Asano Y et al. Kidney Disease Outcomes Quality Initiative (K/DOQI) and the Dialysis Outcomes and Practice Patterns Study (DOPPS): nutrition guidelines, indicators, and practices. Am.J.Kidney Dis. 2004;44:39-46.
13. Donadio C, Consani C, Ardini M et al. Estimate of body water compartments and of body composition in maintenance hemodialysis patients: comparison of single and multifrequency bioimpedance analysis. J.Ren Nutr. 2005; 15:332-344.
14. Mika C, Herpertz-Dahlmann B, Heer M, Holtkamp K. Improvement of nutritional status as assessed by multifrequency BIA during 15 weeks of refeeding in adolescent girls with anorexia nervosa. J. Nutr. 2004; 134:3026-3030.
15. Cheng LT, Tang W, Wang T. Strong association between volume status and nutritional status in peritoneal dialysis patients. Am J Kidney Dis 2005;45:891-902.
16. Cohn JN. Arterial stiffness, vascular disease, and risk of cardiovascular events. Circulation 2006; 113:601-603.
17. Bots ML, Dijk JM, Oren A, Grobbee DE. Carotid intima-media thickness, arterial stiffness and risk of cardiovascular disease: current evidence. J. Hypertens. 2002;20:2317-2325.
18．蒋红樱，程李涛，汪涛。．腹膜透析患者高血压的产生与容量超负荷的关系。．中华肾脏病杂志 2005；21：367-369．
19. Fagugli RM, Pasini P, Quintaliani G et al. Association between extracellular water, left ventricular mass and hypertension in haemodialysis patients. Nephrol. Dial. Transplant. 2003; 18:2332-2338.
20. Khandelwal M, Oreopoulos D. Sodium and volume overload in peritoneal dialysis: limitations of current treatment and possible solutions. Int. Urol. Nephrol. 2004;36:101-107.
21. Fagugli RM, Quintaliani G, Pasini P et al. Blunted nocturnal blood pressure decrease and left-ventricular mass in hypertensive hemodialysis patients. Nephron 2002;91:79-85.
22. Gunal AI, Duman S, Ozkahya M et al. Strict volume control normalizes hypertension in peritoneal dialysis patients. Am.J.Kidney Dis. 2001;37:588-593.
23. Ozkahya M, Toz H, Unsal A et al. Treatment of hypertension in dialysis patients by ultrafiltration: role of cardiac dilatation and time factor. Am J.Kidney Dis. 1999;34:218-221.
24. Charra B, Chazot C, Jean G, Laurent G. Long, slow dialysis. Miner.Electrolyte Metab 1999;25:391-396.
25. Quinlan GJ, Mumby S, Martin GS et al. Albumin influences total plasma antioxidant capacity favorably in patients with acute lung injury. Crit Care Med. 2004;32:755-759.
26. Borawski J, Naumnik B, Pawlak K, Mysliwiec M. Endothelial dysfunction marker von Willebrand factor antigen in haemodialysis patients: associations with pre-dialysis blood pressure and the acute phase response. Nephrol.Dial.Transplant. 2001;16:1442-1447.
27. Konings CJ, Kooman JP, Schonck M et al. Fluid status in CAPD patients is related to peritoneal transport and residual renal function: evidence from a longitudinal study. Nephrol.Dial.Transplant. 2003;18:797-803.
28. Goncalves S, Pecoits-Filho R, Perreto S et al. Associations between renal function, volume status and endotoxaemia in chronic kidney disease patients. Nephrol.Dial.Transplant. 2006;21:2788-2794.
29. Pecoits-Filho R, Lindholm B, Stenvinkel P. The malnutrition, inflammation, and atherosclerosis (MIA) syndrome - the heart of the matter. Nephrol.Dial.Transplant. 2002; 17 Suppl 11:28-31.
30. Stenvinkel P, Alvestrand A. Inflammation in end-stage renal disease: sources, consequences, and therapy. Semin.Dial. 2002;15:329-337.
31. Foley RN, Parfrey PS, Harnett JD et al. Hypoalbuminemia, cardiac morbidity, and mortality in end-stage renal disease. J.Am.Soc.Nephrol. 1996;7:728-736.
32. Wong CS, Hingorani S, Gillen DL et al. Hypoalbuminemia and risk of death in pediatric patients with end-stage renal disease. Kidney Int. 2002;61:630-637.
33. Kalantar-Zadeh K, Kilpatrick RD, Kuwae N et al. Revisiting mortality predictability of serum albumin in the dialysis population: time dependency, longitudinal changes and population-attributable fraction. Nephrol.Dial.Transplant. 2005;20:1880-1888.
34. Benetos A, Rudnichi A, Safar M, Guize L. Pulse pressure and cardiovascular mortality in normotensive and hypertensive subjects. Hypertension 1998;32:560-564.
35．王国宏，胡大一．高血压患者大动脉弹性对冠状动脉血流储备的影响．中华医学杂志 2005；85：54-57．
36. Asmar R, Benetos A, Topouchian J et al. Assessment of arterial distensibility by automatic pulse wave velocity measurement: validation and clinical application study. Hypertension 1995;26:485-490.
37. Boutouyrie P, Tropeano AI, Asmar R et al. Aortic stiffness is an independent predictor of primary coronary events in hypertensive patients: a longitudinal study. Hypertension 2002;39:2085-2090.
38. Cruickshank K, Riste L, Anderson SG et al. Aortic pulse-wave velocity and its relationship to mortality in diabetes and glucose intolerance: an integrated index of vascular function? Circulation 2002; 106:2085-2090.
39. Blacher J, Guerin AP, Pannier B et al. Impact of aortic stiffness on survival in end-stage renal disease. Circulation 1999;99:2434-2439.
40. Guerin A, Blacher J, Pannier B et al. Impact of aortic stiffness attenuation on survival of patients in end-stage renal disease. Circulation 2001; 103:987-992.
41. Danielski M, Ikizler TA, McMonagle E et al. Linkage of hypoalbuminemia, inflammation, and oxidative stress in patients receiving maintenance hemodialysis therapy. Am.J.Kidney Dis. 2003;42:286-294.
42. Dogra GK, Herrmann S, Irish AB, Thomas MA, Watts GF. Insulin resistance, dyslipidaemia, inflammation and endothelial function in nephrotic syndrome. Nephrol.Dial.Transplant. 2002; 17:2220-2225.
43. Joles JA, Stroes ES, Rabelink TJ. Endothelial function in proteinuric renal disease. Kidney Int.Suppl 1999;71:S57-S61.
44. Yang WS, Min WK, Park JS, Kim SB. Effect of increasing serum albumin on serum lipoprotein(a) concentration in patients receiving CAPD. Am.J.Kidney Dis. 1997;30:507-513.
45. Djousse L, Rothman KJ, Cupples A, Arnett DK, Elisson RC. Relation between serum albumin and carotid atherosclerosis The NHLBI Family Heart Study. Stroke 2003;34:53-57.
46. Dart AM, Kingwell B A. Pulse pressure—a review of mechanisms and clinical relevance. J.Am.Coll.Cardiol. 2001;37:975-984.
47. Safar ME, Levy BI, Struijker-Boudier H. Current perspectives on arterial stiffness and pulse pressure in hypertension and cardiovascular diseases. Circulation 2003; 107:2864-2869.
48. Franklin SS, Gustin W, Wong ND et al. Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study. Circulation 1997;96:308-315.
49. Mitchell GF, Vasan RS, Keyes MJ et al. Pulse pressure and risk of new-onset atrial fibrillation. JAMA 2007;297:709-715.
50. Haider AW, Larson MG, Franklin SS, Levy D. Systolic blood pressure, diastolic blood pressure, and pulse pressure as predictors of risk for congestive heart failure in the Framingham Heart Study. Ann.Intern.Med. 2003;138:10-16.
51. Franklin SS, Sutton-Tyrrell K, Belle SH, Weber MA, Kuller LH. The importance of pulsatile components of hypertension in predicting carotid stenosis in older adults. J.Hypertens. 1997; 15:1143-1150.
52. Haider AW, Larson MG, Franklin SS, Levy D. Systolic blood pressure, diastolic blood pressure, and pulse pressure as predictors of risk for congestive heart failure in the Framingham Heart Study. Ann.Intern.Med. 2003;138:10-16.
53. Van Bortel LM, Struijker-Boudier HA, Safar ME. Pulse pressure, arterial stiffness, and drug treatment of hypertension. Hypertension 2001;38:914-921.
54. Strandberg TE, Pitkala K. What is the most important component of blood pressure:systolic, diastolic or pulse pressure? Curr.Opin.Nephrol.Hypertens. 2003;12:293-297.
55. Lip GY, Blann AD. von Willebrand factor and its relevance to cardiovascular disorders. Br.Heart J. 1995;74:580-583.
56. Blann AD. Von Willebrand factor and forearm blood flow as indicators of endothelial dysfunction. Atherosclerosis 2004; 176:423-424.
57. Cameron JS. The nephrotic syndrome and its complications. Am.J.Kidney Dis. 1987;10:157-171.
58. Joven J, Espinel E, Simo JM et al. The influence of hypoalbuminemia in the generation of nephrotic hyperlipidemia. Atherosclerosis 1996; 126:243-252.
59. Shoji T, Nishizawa Y, Nishitani H, Yamakawa M, Morii H. Roles of hypoalbuminemia and lipoprotein lipase on hyperlipoproteinemia in continuous ambulatory peritoneal dialysis. Metabolism 1991 ;40:1002-1008.
60. Scolnik D, Balfe JW. Initial hypoalbuminemia and hyperlipidemia persist during chronic peritoneal dialysis in children. Perit.Dial.Int. 1993;13:136-139.
61. Khandelwal M, Oreopoulos D. Sodium and volume overload in peritoneal dialysis: limitations of current treatment and possible solutions. Int.Urol.Nephrol. 2004;36:101 -107.
62．唐利军，程李涛，胡昭，毕书红，唐雯，汪涛．CAPD患者低白蛋白血症与脉压的关系。．中华肾脏病杂志 2006；22：641-642．
63. Dart AM, Kingwell BA. Pulse pressure-a review of mechanisms and clinical relevance. J. Am. Coll. Cardiol. 2001;37:975-984.
64. Assmann G, Cullen P, Evers T, Petzinna D, Schulte H. Importance of arterial pulse pressure as predictor of coronary heart disease risk in PROCAM. Eur. Heart J. 2005;26:2120-2126.
65. Davies SJ, Woodrow G, Donovan K et al. Icodextrin improves the fluid status of peritoneal dialysis patients: results of a double-blind randomized controlled trial. J. Am. Soc. Nephrol. 2003; 14:2338-2344.
66. Dart AM, Kingwell BA. Pulse pressure-a review of mechanisms and clinical relevance. J. Am. Coll. Cardiol. 2001;37:975-984.
67．俞雨生．容量负荷对腹膜透析的影响。．肾脏病与透析肾移植杂志 2004；13：378-381．
68．李伟，唐珊珊，刘怡芝，郭颖超，穆柯晓．容量控制对腹膜透析患者体液平衡的影响。．中国血液净化杂志 2005；4：607-609．
69．王瑞敏，马岩，胜彦婷，赵黎佳，杜凤和，汪涛．腹膜透析患者容量控制对血压的影响。．临床内科杂志 2005；22：519-521．
70. Pecoits-Filho R, Lindholm B, Stenvinkel P. The malnutrition, inflammation, and atherosclerosis (MIA) syndrome - the heart of the matter. Nephrol.Dial.Transplant. 2002; 17 Suppl 11:28-31.
71. Stenvinkel P, Alvestrand A. Inflammation in end-stage renal disease: sources, consequences, and therapy. Semin.Dial. 2002;15:329-337.
2. Chung SH, Lindholm B, Lee HB. Influence of initial nutritional status on continuous ambulatory peritoneal dialysis patient survival. Perit.Dial.Int. 2000;20:19-26.
3. Bergstrom J, Lindholm B. Malnutrition, cardiac disease, and mortality: an integrated point of view. Am J.Kidney Dis. 1998;32:834-841.
4. Fung F, Sherrard DJ, Gillen DL et al. Increased risk for cardiovascular mortality among malnourished end-stage renal disease patients. Am J.Kidney Dis. 2002;40:307-314.
5. Cooper BA, Penne EL, Bartlett LH, Pollock CA. Protein malnutrition and hypoalbuminemia as predictors of vascular events and mortality in ESRD. AmJ.Kidney Dis. 2004;43:61-66.
6. Covic A, Gusbeth-Tatomir P, Goldsmith DJ. Arterial stiffness in renal patients: an update. Am J Kidney Dis 2005;45:965-977.
7. Asmar R, Rudnichi A, Blacher J, London GM, Safar ME. Pulse pressure and aortic pulse wave are markers of cardiovascular risk in hypertensive populations. Am J Hypertens. 2001;14:91-97.
8. Laurent S, Boutouyrie P, Asmar R et al. Aortic stiffness is an independent risk predictor of all-cause and mortality in hypertensive patients. Hypertension 2001;37:1236-1241.
9. Hansen TW, Staessen JA, Torp-Pedersen C et al. Prognostic value of aortic pulse wave velocity as index of arterial stiffness in the general population.Circulation 2006; 113:664-670.
10. Laurent S. Surrogate measures of arterial stiffness: do they have additive predictive value or are they only surrogates of a surrogate? Hypertension 2006;47:325-326.
11. O'Rourke MF, Staessen JA, Vlachojannis JA, Duprez D, Plante GE. Clinical application of arterial stiffness:definitions and reference values. Am J Hypertens. 2002; 15:426-444.
12. Combe C, McCullough KP, Asano Y et al. Kidney Disease Outcomes Quality Initiative (K/DOQI) and the Dialysis Outcomes and Practice Patterns Study (DOPPS): nutrition guidelines, indicators, and practices. Am.J.Kidney Dis. 2004;44:39-46.
13. Donadio C, Consani C, Ardini M et al. Estimate of body water compartments and of body composition in maintenance hemodialysis patients: comparison of single and multifrequency bioimpedance analysis. J.Ren Nutr. 2005; 15:332-344.
14. Mika C, Herpertz-Dahlmann B, Heer M, Holtkamp K. Improvement of nutritional status as assessed by multifrequency BIA during 15 weeks of refeeding in adolescent girls with anorexia nervosa. J. Nutr. 2004; 134:3026-3030.
15. Cheng LT, Tang W, Wang T. Strong association between volume status and nutritional status in peritoneal dialysis patients. Am J Kidney Dis 2005;45:891-902.
16. Cohn JN. Arterial stiffness, vascular disease, and risk of cardiovascular events. Circulation 2006; 113:601-603.
17. Bots ML, Dijk JM, Oren A, Grobbee DE. Carotid intima-media thickness, arterial stiffness and risk of cardiovascular disease: current evidence. J. Hypertens. 2002;20:2317-2325.
18．蒋红樱，程李涛，汪涛。．腹膜透析患者高血压的产生与容量超负荷的关系。．中华肾脏病杂志 2005；21：367-369．
19. Fagugli RM, Pasini P, Quintaliani G et al. Association between extracellular water, left ventricular mass and hypertension in haemodialysis patients. Nephrol. Dial. Transplant. 2003; 18:2332-2338.
20. Khandelwal M, Oreopoulos D. Sodium and volume overload in peritoneal dialysis: limitations of current treatment and possible solutions. Int. Urol. Nephrol. 2004;36:101-107.
21. Fagugli RM, Quintaliani G, Pasini P et al. Blunted nocturnal blood pressure decrease and left-ventricular mass in hypertensive hemodialysis patients. Nephron 2002;91:79-85.
22. Gunal AI, Duman S, Ozkahya M et al. Strict volume control normalizes hypertension in peritoneal dialysis patients. Am.J.Kidney Dis. 2001;37:588-593.
23. Ozkahya M, Toz H, Unsal A et al. Treatment of hypertension in dialysis patients by ultrafiltration: role of cardiac dilatation and time factor. Am J.Kidney Dis. 1999;34:218-221.
24. Charra B, Chazot C, Jean G, Laurent G. Long, slow dialysis. Miner.Electrolyte Metab 1999;25:391-396.
25. Quinlan GJ, Mumby S, Martin GS et al. Albumin influences total plasma antioxidant capacity favorably in patients with acute lung injury. Crit Care Med. 2004;32:755-759.
26. Borawski J, Naumnik B, Pawlak K, Mysliwiec M. Endothelial dysfunction marker von Willebrand factor antigen in haemodialysis patients: associations with pre-dialysis blood pressure and the acute phase response. Nephrol.Dial.Transplant. 2001;16:1442-1447.
27. Konings CJ, Kooman JP, Schonck M et al. Fluid status in CAPD patients is related to peritoneal transport and residual renal function: evidence from a longitudinal study. Nephrol.Dial.Transplant. 2003;18:797-803.
28. Goncalves S, Pecoits-Filho R, Perreto S et al. Associations between renal function, volume status and endotoxaemia in chronic kidney disease patients. Nephrol.Dial.Transplant. 2006;21:2788-2794.
29. Pecoits-Filho R, Lindholm B, Stenvinkel P. The malnutrition, inflammation, and atherosclerosis (MIA) syndrome - the heart of the matter. Nephrol.Dial.Transplant. 2002; 17 Suppl 11:28-31.
30. Stenvinkel P, Alvestrand A. Inflammation in end-stage renal disease: sources, consequences, and therapy. Semin.Dial. 2002;15:329-337.
31. Foley RN, Parfrey PS, Harnett JD et al. Hypoalbuminemia, cardiac morbidity, and mortality in end-stage renal disease. J.Am.Soc.Nephrol. 1996;7:728-736.
32. Wong CS, Hingorani S, Gillen DL et al. Hypoalbuminemia and risk of death in pediatric patients with end-stage renal disease. Kidney Int. 2002;61:630-637.
33. Kalantar-Zadeh K, Kilpatrick RD, Kuwae N et al. Revisiting mortality predictability of serum albumin in the dialysis population: time dependency, longitudinal changes and population-attributable fraction. Nephrol.Dial.Transplant. 2005;20:1880-1888.
34. Benetos A, Rudnichi A, Safar M, Guize L. Pulse pressure and cardiovascular mortality in normotensive and hypertensive subjects. Hypertension 1998;32:560-564.
35．王国宏，胡大一．高血压患者大动脉弹性对冠状动脉血流储备的影响．中华医学杂志 2005；85：54-57．
36. Asmar R, Benetos A, Topouchian J et al. Assessment of arterial distensibility by automatic pulse wave velocity measurement: validation and clinical application study. Hypertension 1995;26:485-490.
37. Boutouyrie P, Tropeano AI, Asmar R et al. Aortic stiffness is an independent predictor of primary coronary events in hypertensive patients: a longitudinal study. Hypertension 2002;39:2085-2090.
38. Cruickshank K, Riste L, Anderson SG et al. Aortic pulse-wave velocity and its relationship to mortality in diabetes and glucose intolerance: an integrated index of vascular function? Circulation 2002; 106:2085-2090.
39. Blacher J, Guerin AP, Pannier B et al. Impact of aortic stiffness on survival in end-stage renal disease. Circulation 1999;99:2434-2439.
40. Guerin A, Blacher J, Pannier B et al. Impact of aortic stiffness attenuation on survival of patients in end-stage renal disease. Circulation 2001; 103:987-992.
41. Danielski M, Ikizler TA, McMonagle E et al. Linkage of hypoalbuminemia, inflammation, and oxidative stress in patients receiving maintenance hemodialysis therapy. Am.J.Kidney Dis. 2003;42:286-294.
42. Dogra GK, Herrmann S, Irish AB, Thomas MA, Watts GF. Insulin resistance, dyslipidaemia, inflammation and endothelial function in nephrotic syndrome. Nephrol.Dial.Transplant. 2002; 17:2220-2225.
43. Joles JA, Stroes ES, Rabelink TJ. Endothelial function in proteinuric renal disease. Kidney Int.Suppl 1999;71:S57-S61.
44. Yang WS, Min WK, Park JS, Kim SB. Effect of increasing serum albumin on serum lipoprotein(a) concentration in patients receiving CAPD. Am.J.Kidney Dis. 1997;30:507-513.
45. Djousse L, Rothman KJ, Cupples A, Arnett DK, Elisson RC. Relation between serum albumin and carotid atherosclerosis The NHLBI Family Heart Study. Stroke 2003;34:53-57.
46. Dart AM, Kingwell B A. Pulse pressure—a review of mechanisms and clinical relevance. J.Am.Coll.Cardiol. 2001;37:975-984.
47. Safar ME, Levy BI, Struijker-Boudier H. Current perspectives on arterial stiffness and pulse pressure in hypertension and cardiovascular diseases. Circulation 2003; 107:2864-2869.
48. Franklin SS, Gustin W, Wong ND et al. Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study. Circulation 1997;96:308-315.
49. Mitchell GF, Vasan RS, Keyes MJ et al. Pulse pressure and risk of new-onset atrial fibrillation. JAMA 2007;297:709-715.
50. Haider AW, Larson MG, Franklin SS, Levy D. Systolic blood pressure, diastolic blood pressure, and pulse pressure as predictors of risk for congestive heart failure in the Framingham Heart Study. Ann.Intern.Med. 2003;138:10-16.
51. Franklin SS, Sutton-Tyrrell K, Belle SH, Weber MA, Kuller LH. The importance of pulsatile components of hypertension in predicting carotid stenosis in older adults. J.Hypertens. 1997; 15:1143-1150.
52. Haider AW, Larson MG, Franklin SS, Levy D. Systolic blood pressure, diastolic blood pressure, and pulse pressure as predictors of risk for congestive heart failure in the Framingham Heart Study. Ann.Intern.Med. 2003;138:10-16.
53. Van Bortel LM, Struijker-Boudier HA, Safar ME. Pulse pressure, arterial stiffness, and drug treatment of hypertension. Hypertension 2001;38:914-921.
54. Strandberg TE, Pitkala K. What is the most important component of blood pressure:systolic, diastolic or pulse pressure? Curr.Opin.Nephrol.Hypertens. 2003;12:293-297.
55. Lip GY, Blann AD. von Willebrand factor and its relevance to cardiovascular disorders. Br.Heart J. 1995;74:580-583.
56. Blann AD. Von Willebrand factor and forearm blood flow as indicators of endothelial dysfunction. Atherosclerosis 2004; 176:423-424.
57. Cameron JS. The nephrotic syndrome and its complications. Am.J.Kidney Dis. 1987;10:157-171.
58. Joven J, Espinel E, Simo JM et al. The influence of hypoalbuminemia in the generation of nephrotic hyperlipidemia. Atherosclerosis 1996; 126:243-252.
59. Shoji T, Nishizawa Y, Nishitani H, Yamakawa M, Morii H. Roles of hypoalbuminemia and lipoprotein lipase on hyperlipoproteinemia in continuous ambulatory peritoneal dialysis. Metabolism 1991 ;40:1002-1008.
60. Scolnik D, Balfe JW. Initial hypoalbuminemia and hyperlipidemia persist during chronic peritoneal dialysis in children. Perit.Dial.Int. 1993;13:136-139.
61. Khandelwal M, Oreopoulos D. Sodium and volume overload in peritoneal dialysis: limitations of current treatment and possible solutions. Int.Urol.Nephrol. 2004;36:101 -107.
62．唐利军，程李涛，胡昭，毕书红，唐雯，汪涛．CAPD患者低白蛋白血症与脉压的关系。．中华肾脏病杂志 2006；22：641-642．
63. Dart AM, Kingwell BA. Pulse pressure-a review of mechanisms and clinical relevance. J. Am. Coll. Cardiol. 2001;37:975-984.
64. Assmann G, Cullen P, Evers T, Petzinna D, Schulte H. Importance of arterial pulse pressure as predictor of coronary heart disease risk in PROCAM. Eur. Heart J. 2005;26:2120-2126.
65. Davies SJ, Woodrow G, Donovan K et al. Icodextrin improves the fluid status of peritoneal dialysis patients: results of a double-blind randomized controlled trial. J. Am. Soc. Nephrol. 2003; 14:2338-2344.
66. Dart AM, Kingwell BA. Pulse pressure-a review of mechanisms and clinical relevance. J. Am. Coll. Cardiol. 2001;37:975-984.
67．俞雨生．容量负荷对腹膜透析的影响。．肾脏病与透析肾移植杂志 2004；13：378-381．
68．李伟，唐珊珊，刘怡芝，郭颖超，穆柯晓．容量控制对腹膜透析患者体液平衡的影响。．中国血液净化杂志 2005；4：607-609．
69．王瑞敏，马岩，胜彦婷，赵黎佳，杜凤和，汪涛．腹膜透析患者容量控制对血压的影响。．临床内科杂志 2005；22：519-521．
70. Pecoits-Filho R, Lindholm B, Stenvinkel P. The malnutrition, inflammation, and atherosclerosis (MIA) syndrome - the heart of the matter. Nephrol.Dial.Transplant. 2002; 17 Suppl 11:28-31.
71. Stenvinkel P, Alvestrand A. Inflammation in end-stage renal disease: sources, consequences, and therapy. Semin.Dial. 2002;15:329-337.