Abstract
Recently, a genetic predisposition to susceptibility to diabetic nephropathy has been suggested. In 1994 Marre et al reported that a Deletion (D)/Insertion (I) polymorphism in the angiotensin I converting enzyme (ACE) gene is related to the development of diabetic nephropathy in insulindependent diabetes mellitus. This theory has been questioned by Schmidt and others, and a consistent conclusion has not been reached. The reason for these contradictory results are thought to be due to the different clinical states of patients tested, especially with respect to blood sugar control.
In this study we examined the relationship between the D/I polymorphism of the ACE gene and diabetic nephropathy in non-insulin-dependent diabetic patients with proliferative retinopathy (n=45), who were thought to have been exposed to a hyperglycemic state long enough to suffer from microangiopathy. They were divided into two subgroups: 24 patients with nephropathy (albumin excretion rate: AER≥20μg/min) and 21 patients without nephropathy (AER<20μg/min). There was no difference between these subgroups in the duration of diabetes, the level of HbA1c, or average blood pressure in the latest year, nor in other clinical characteristics. However, patients without nephropathy had the I allele more often than those with nephropathy (P=0.025). AER was lowest in the II genotype and highest in the DD genotype but the difference was not significant (P=0.07).
From the findings of the present study, it was concluded that the II genotype of the ACE gene is a marker for reduced risk for diabetic nephropathy.
