组织激肽释放酶基因多态性A1789G 对高血压患者血浆肌酐水平的影响

目的:探讨组织激肽释放酶基因多态性对高血压患者血浆肌酐水平的影响.方法:用聚合酶链反应-限制性片段长度多态性( PCR-RFLP)方法对 733 例高血压患者的组织激肽释放酶基因 A1789G 多态位点进行基因分型,用线性回归模型分析基因型与血浆肌酐水平之间的关系,用方差分析分析基因型和血压对血浆肌酐水平的交互影响.结果:携带突变型等位基因1789G(基因型AG或GG)高血压患者较携带野生型等位基因A1789(基因型AA)患者的血浆肌酐水平明显升高,且血浆肌酐水平随着血压的升高而升高.结论:组织激肽释放酶基因多态性对高血压患者的血浆肌酐水平产生明显影响,A1789G 多态位点是高血压患者血浆肌酐清除率下降的一个危险因素.

Effects of human tissue kallikrein gene A1789G polymorphism on plasma creatinine levels in patients with essential hypertension

AIM: To investigate the effect of the human tissue kallikrein gene (hKLK1) polymorphism on plasma creatinine levels in hypertensive subjects. METHODS: The hKLK1 A1789G polymorphism was genotyped by PCR-restriction fragment length polymorphism (RFLP) in 733 hypertensive subjects. The relationship between genotype and plasma creatinine level was performed by a multiple regression analysis. The interactive effect of genotype and blood pressure on the plasma creatinine level was accessed by ANOVA. RESULTS: Multiple regression analysis showed that the plasma creatinine level was significantly higher in the subjects with mutant allele G (AG or GG genotype) than in those with wild allele A (AA genotype) (P=0.009 and P=0.046, respectively). ANOVA indicated that the AG and GG genotype individuals had high plasma creatinine levels in SBP and DBP Compared with AA genotype individuals, and the plasma creatinine level increased with blood pressure rises (P<0.05). CONCLUSION: The hKLK1 A1789G polymorphism influences plasma creatinine level, and the A1789→G variation is a risk factor in renal plasma creatinine clearance rate decline in hypertensive individuals.