目的通过观察不同血液净化方式的联合应用对血液透析患者血清中骨代谢指标及骨质疏松患病率的影响,来评价血液透析方式的不同组合对血液透析患者矿物质和骨异常(mineral and bone disorder,MBD)的影响。方法维持性血液透析患者90例,随...目的通过观察不同血液净化方式的联合应用对血液透析患者血清中骨代谢指标及骨质疏松患病率的影响,来评价血液透析方式的不同组合对血液透析患者矿物质和骨异常(mineral and bone disorder,MBD)的影响。方法维持性血液透析患者90例,随机分为血液透析组(对照组或HD组)、血液透析加血液透析滤过组(HD+HDF组)、血液透析加血液灌流组(HD+HP组),每组30例,观察6个月,比较组内及组间6个月前后血钙、血磷、全段甲状旁腺激素(intact parathyroid hormone,iPTH)、成纤维生长因子23(fibroblast growth factor23,FGF-23)、β-I型胶原羧基末端肽(β-Type I collagen carboxy-terminal peptide,β-CTX)、I型前胶原氨基末端肽(Type I procollagen amino-terminal peptide,PINP)、骨质疏松患病率等指标的变化来评价不同透析方式的组合对血液透析患者MBD的影响。结果组内自身前后比较:HD组血磷[(2.21±0.55)mmol/l vs.(2.64±1.04)mmol/l,t=2.047、P=0.049]、iPTH[(427.7±44.00)pg/ml vs.(452.1±43.00)pg/ml,t=2.140,P=0.038]变化有统计学差异;HD+HDF组的iPTH下降有统计学差异[(465.3±43.02)pg/ml vs.(431.0±37.39)pg/ml,t=3.298,P=0.007];HD+HP组的iPTH[(457.4±60.01)pg/mlvs.(389.1±29.89)pg/ml,t=5.598,P=0.001)、β-CTX[(2.73±1.16)ng/ml vs.(2.13±1.51)ng/ml,t=2.142,P=0.045];PINP[(157.92±31.16)ng/mlvs.(140.76±36.13)ng/ml,t=2.106,P=0.047];FGF-23[(461.16±101.69)ng/ml vs.(397.30±63.18)ng/ml,t=2.922,P=0.011]下降均有统计学意义。组间比较6个月后,HD+HDF组PINP为(147.33±40.72)ng/ml,HD组PINP为(165.32±43.11)ng/ml,二者比较有统计学差异(t=1.969,P=0.048);HD+HDF组FGF-23(465.38±101.36)ng/ml,HD组FGF-23(403.56±96.81)ng/ml,二者比较HD+HDF组更低,有统计学差异(t=2.415,P=0.019);组间比较6个月后,HD+HP组与HD组比较,血磷[(2.02±0.81)mmol/L vs.(2.64±1.04)mmol/L,t=3.221,P=0.003]、iPTH[(389.1±29.89)pg/ml vs.(452.1±43.0)pg/ml,t=6.661,P=0.005]、β-CTX[(2.13±1.51)ng/ml vs.(2.95±1.28)ng/ml,t=2.278,P=0.031]、PINP[(140.76±36.13)ng/ml vs.(165.32±43.11)ng/ml,t=2.339,P=0.028]、FGF-23[(397.30±63.18)ng/ml vs.(465.38±101.36)ng/ml,t=3.114,P=0.003],上述指标HD+HP组较HD组更低,均有统计学意义;组间比较6个月后,HD+HP组与HD+HDF组比较iPTH分别为(389.1±29.89)ng/ml、(431.0±37.39)ng/ml,HD+HP组更低,有统计学意义(t=7.303,P=0.000)。骨质疏松患病率:对照组观察期后骨质疏松和骨量低下的病例数增加,但无统计学意义;HD+HDF组、HD+HP组骨质疏松的病例数有减少,亦无统计学意义(P>0.05)。结论不同的血液透析方式的联合使用对维持性血液透析患者MBD影响不同;血液透析联合血液透析滤过或血液灌流的治疗方式较单纯血液透析有利MBD的改善;血液透析联合血液灌流在骨代谢指标的改善方面更具优势。展开更多
Adiponectin plays an important role in the development of hypertension, atherosclerosis, and cardiomyocyte hypertrophy, but very little was known about the influence of serum adiponectin or the adiponectin gene polymo...Adiponectin plays an important role in the development of hypertension, atherosclerosis, and cardiomyocyte hypertrophy, but very little was known about the influence of serum adiponectin or the adiponectin gene polymorphism on myocardial fibrosis. Our study investigates the influence of the SNP +45 polymorphism of the adiponectin gene and serum levels of adiponectin on myocardial fibrosis in patients with essential hypertension. A case-control study was conducted on 165 hypertensive patients and 126 normotensive healthy controls. The genotypes of adiponectin gene polymorphisms were detected by the polymerase chain reaction (PCR) method. Serum concentrations of procollagen were measured by a double antibody sandwich enzyme-linked immunosorbent assay (ELISA) in all subjects. The integrated backscatter score (IBS) was measured in the left ventricular myocardium using echocardiography. The serum levels of adiponectin in hypertensive patients were significantly lower than those in the normal control group ((2.69±1.0) μg/ml vs. (4.21±2.89) μg/ml, respectively, P<0.001). The serum levels of type-I procollagen carboxyl end peptide (PICP) and type-III procollagen ammonia cardinal extremity peptide (PIIINP) in the hypertension group were significantly higher than those in the control group. In the hypertension group, serum levels of adiponectin were significantly and negatively related to the average acoustic intensity and corrected acoustic intensity of the myocardium (r=0.46 and 0.61, respectively, P<0.05 for both). The serum levels of PICP and PIIINP were significantly different among the three genotypes of SNP +45 (P<0.01). Logistic regression analyses showed that sex and genotype (GG+GT) were the major risk factors of myocardial fibrosis in hypertensive patients (OR=5.343 and 3.278, respectively, P<0.05). These data suggest that lower levels of adiponectin and SNP +45 polymorphism of the adiponectin gene are likely to play an important role in myocardial fibrosis in hypertensive patients.展开更多
基金Project supported by the Natural Science Foundation of Shandong Province, China (No. ZR2012HL19)the Science and Technology Development Plan of Tai’an City, China (No. 20113096)
文摘Adiponectin plays an important role in the development of hypertension, atherosclerosis, and cardiomyocyte hypertrophy, but very little was known about the influence of serum adiponectin or the adiponectin gene polymorphism on myocardial fibrosis. Our study investigates the influence of the SNP +45 polymorphism of the adiponectin gene and serum levels of adiponectin on myocardial fibrosis in patients with essential hypertension. A case-control study was conducted on 165 hypertensive patients and 126 normotensive healthy controls. The genotypes of adiponectin gene polymorphisms were detected by the polymerase chain reaction (PCR) method. Serum concentrations of procollagen were measured by a double antibody sandwich enzyme-linked immunosorbent assay (ELISA) in all subjects. The integrated backscatter score (IBS) was measured in the left ventricular myocardium using echocardiography. The serum levels of adiponectin in hypertensive patients were significantly lower than those in the normal control group ((2.69±1.0) μg/ml vs. (4.21±2.89) μg/ml, respectively, P<0.001). The serum levels of type-I procollagen carboxyl end peptide (PICP) and type-III procollagen ammonia cardinal extremity peptide (PIIINP) in the hypertension group were significantly higher than those in the control group. In the hypertension group, serum levels of adiponectin were significantly and negatively related to the average acoustic intensity and corrected acoustic intensity of the myocardium (r=0.46 and 0.61, respectively, P<0.05 for both). The serum levels of PICP and PIIINP were significantly different among the three genotypes of SNP +45 (P<0.01). Logistic regression analyses showed that sex and genotype (GG+GT) were the major risk factors of myocardial fibrosis in hypertensive patients (OR=5.343 and 3.278, respectively, P<0.05). These data suggest that lower levels of adiponectin and SNP +45 polymorphism of the adiponectin gene are likely to play an important role in myocardial fibrosis in hypertensive patients.
