The punpose of the research is 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. Ninety two cases with diabetes nephropathy were classified according to the genotype of the ACE gene into three groups:31 cases with II genotypes, 30 with ID and 31 with DD. Mean arterial blood pressure(MABP), urinary albuminexcretion rate(UAER), creatinine clearance rate(Ccr)and ACE levels were measured before and after the six month treatment of benazepril(no differences in drug dose between the groups).Initiation of the 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(UAER 58.6%, MABP 2.87 kPa, ACE 72.3 %), compared with patients with either ID or DD genotype(P<0.01, respectivly). A mild decline in the creatinine clearance rate was seen in all groups after the initiation of benazepril, but the change was highest in DD group and lowest(P<0.05)in II group. A multiple linear regression analysis revealed that the ACE gene polymorphism influenced the decline in albuminuria after initiation of ACE inhibition(R2=0.72, P<0.001). The patients with II genotype are particularly susceptible to commonly advocated renoprotective treatment.
