Oobjective To test the potential role of an insertion/deletion polymorphism of angiotensin converting enzyme (ACE) gene on the renoprotective responsiveness to benazepril in type 2 diabetes mellitus with nephropath...Oobjective To test the potential role of an insertion/deletion polymorphism of angiotensin converting enzyme (ACE) gene on the renoprotective responsiveness to benazepril in type 2 diabetes mellitus with nephropathy Methods The insertion/deletion polymorphisms of ACE gene were determined by polymerase chain reaction(PCR) Ninety cases with diabetes nephropathy were classified according to the genotype of the ACE gene into 30 cases with II genotypes, 29 with ID and 31 with DD Mean arterial blood pressure (MABP), urinary albumin excretion rate (UAER), serum creatinine (Scr) and ACE levels were measured before and after the six month treatment of benazepril (no differences in drug dose between groups) Results At baseline the three groups with different genotypes were similar with regard to sex, age, duration of diabetes, frequency of retinopathy, body mass index, HbA 1c, MABP, UAER, serum creatinine, total cholesterol, triglyceride, high density lipoprotein, low density lipoprotein, insulin dose The dose of benazepril and the number of patients receiving nifedipine after starting ACEI were also similar in the patients with II, ID, DD genotypes, respectively The serum levels of ACE in patients with DD genotype were the highest, the intermediate with ID and the lowest with II genotype ( P <0 05) Initiation of 6 month treatment with benazepril induced a significant drop in MABP,UAER and ACE levels in all three groups ( P <0 05),but the reduction was significantly greater in patients with II genotype (UAER57 9%, MABP21 4?mm?Hg, ACE74 8%), compared to patients with either ID or DD genotype ( P <0 01, respectivly) A mild increase in the serum creatinine was seen in all groups after the initiation of benazepril, but the rate of increase in DD group was the highest (8 9%) and in II group lowest (5 4%) ( P <0 05) A multiple linear regression analysis revealed that the ACE gene polymorphism influenced the decline in albuminuria after initiation of ACE inhibition (R 2=0 展开更多
文摘Oobjective To test the potential role of an insertion/deletion polymorphism of angiotensin converting enzyme (ACE) gene on the renoprotective responsiveness to benazepril in type 2 diabetes mellitus with nephropathy Methods The insertion/deletion polymorphisms of ACE gene were determined by polymerase chain reaction(PCR) Ninety cases with diabetes nephropathy were classified according to the genotype of the ACE gene into 30 cases with II genotypes, 29 with ID and 31 with DD Mean arterial blood pressure (MABP), urinary albumin excretion rate (UAER), serum creatinine (Scr) and ACE levels were measured before and after the six month treatment of benazepril (no differences in drug dose between groups) Results At baseline the three groups with different genotypes were similar with regard to sex, age, duration of diabetes, frequency of retinopathy, body mass index, HbA 1c, MABP, UAER, serum creatinine, total cholesterol, triglyceride, high density lipoprotein, low density lipoprotein, insulin dose The dose of benazepril and the number of patients receiving nifedipine after starting ACEI were also similar in the patients with II, ID, DD genotypes, respectively The serum levels of ACE in patients with DD genotype were the highest, the intermediate with ID and the lowest with II genotype ( P <0 05) Initiation of 6 month treatment with benazepril induced a significant drop in MABP,UAER and ACE levels in all three groups ( P <0 05),but the reduction was significantly greater in patients with II genotype (UAER57 9%, MABP21 4?mm?Hg, ACE74 8%), compared to patients with either ID or DD genotype ( P <0 01, respectivly) A mild increase in the serum creatinine was seen in all groups after the initiation of benazepril, but the rate of increase in DD group was the highest (8 9%) and in II group lowest (5 4%) ( P <0 05) A multiple linear regression analysis revealed that the ACE gene polymorphism influenced the decline in albuminuria after initiation of ACE inhibition (R 2=0
