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遗传和环境因素对高血压病患者肾脏损害的影响 被引量:2

Effects of Genetic and Environmental Factors on the Development of Renal Damage in Patients With Essential Hypertension
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摘要 目的探讨血管紧张素ⅡⅠ型受体 (AT1R)A/C116 6多态性、纤溶酶原激活物抑制剂 - 1(PAI - 1) 4G/5G多态性和环境因素与高血压性肾脏损害发生的关系。 方法高血压病患者 96例 ,采集详尽临床和生化资料。采用等位基因特异性寡核苷酸探针杂交方法分析AT1R基因型和PAI - 1基因型。通过多因素Logistic回归分析识别高血压病人群肾脏损害发生的危险因素。 结果PAI- 1基因型与肾脏功能无显著性关系 (P >0 .0 5 ) ;AT1R基因型与肾脏功能显著相关 (P <0 .0 1) ;Logistic回归分析中 ,AT1RAC基因型、糖尿病和高龄是高血压病并发肾脏损害的三个独立危险因素 (OR值和P值分别为 4.2 9和 0 .0 479,4.6 7和 0 .0 410 ,3 .5 2和 0 .0 0 94)。 结论AT1RAC基因型、糖尿病和高龄为高血压病人群肾脏损害发生的独立危险因素。 Objective To investigate the influences of angiotensin Ⅱ type 1 receptor (AT 1R) A/C 1166 polymorphism, plasminogen activator inhibitor-1 (PAI-1) 4G/5G polymorphism and environmental factors on the development of renal damage in a population with essential hypertension (EH). Methods 96 patients with EH were randomly enrolled in the study. AT 1R and PAI-1 genotypes were analyzed by the allele specific oligonucleotide hybridization technique. Multivariate logistic regression analysis was performed to identify risk factors that may influence the occurrence of renal damage in patients with EH. Results PAI-1 genotypes were not significantly associated with the renal function in patients with EH(P>0.05). AT 1R genotypes were significantly related to renal function in the same subjects (P<0.01). AT 1R genotypes, diabetes mellitus and age ≥70 years were three independent renal damage risk factors (respective odds ratios and P-values:4.29 and 0.0479,4.67 and 0.0410,3.52 and 0.0094). Conclusion AT 1R genotypes, diabetes mellitus and age are independent predictors for renal damage in a population with EH.
出处 《上海第二医科大学学报》 CAS CSCD 2000年第6期521-523,543,共4页 Acta Universitatis Medicinalis Secondae Shanghai
关键词 高血压病 肾脏损害 血管紧张素ⅡⅠ型受体基因型 纤溶酶原激活物抑制剂-1基因型 危险因素 essential hypertension renal damage angiotensinⅡtype 1 receptor genotypes plasminogen activator inhibitor-1 genotypes risk factors
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参考文献5

  • 1Doria A,Diabetologia,1997年,40卷,11期,1293页
  • 2Kagami S,Kidney Int,1997年,51卷,3期,664页
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