Diabetic nephropathy is an important cause of end-stage renal disease in Korea and associated with morbidity and mortality of diabetes mellitus patients. Renin-angiotensin system plays an important role in pathogenetic mechanism of renal injury associated with angiotensin II. Its activity is controlled by angiotensin-converting enzyme(ACE) activity. Plasma and tissue ACE levels can be under the control of an Insertion/Deletion(I/D) polymorphism of the ACE gene, and this polymorphism has shown to be associated with the risk of various complications of diabetes mellitus. So we evaluate the distribution of ACE gene polymorphism in various conditions of diabetes mellitus, diabetic nephropathy, end stage renal disease(ESRD), other microvascular complications such as diabetic neuropathy and diabetic retinopathy, and ischemic heart disease or left ventricular hypertrophy. ACE genotype was determined in 171 diabetes mellitus patients(64 without nephropathy, 34 with nephropathy, 73 ESRD) and 120 non-diabetic controls by DNA PCR. The results were as follow. 1) Patients population consist of 171 diabetes mellitus and male to female ratio was 81:90, mean age 55.2+/-14.1 years old. 120 nondiabetic controls were male to female ratio 62:58, mean age 46.1+/-15.1. The age and sex distribution in control and patient group was not significantly different. 2) ACE genotypes in whole population were 29.9% DD genotype, 47.8% ID genotype, 22.3% II genotype. ID genotype was most frequently encountered, and DD genotype was found frequently in diabetic nephropathy group compare to non-nephropathy group(41.1% vs. 17.2%, P<0.05). 3) Microvascular complications were not significantly associated with ACE gene polymorphism. 4) The genotype distribution in diabetes mellitus patients according to the prevalance of LVH or ischemic heart disease showed no significant association with ACE genotype. From the above results, we concluded that ACE gene polymorphism was important in the progression of diabetic nephropathy, and DD genotype was considered to be a risk factor of disease progression.