BACKGROUND: Albuminuria is a risk factor for progression of diabetic nephropathy. Antihypertensive treatment, especially angiotensin converting enzyme (ACE) inhibition, has been shown to reduce albuminuria and to ameliorate progression of diabetic nephropathy in IDDM patients. Recently, an insertion (I)/deletion (D) polymorphism of the ACE gene (ACE/ID) has been shown to influence the antiproteinuric efficacy of ACE inhibition in non-diabetic renal disease and the deterioration in kidney function in both non-diabetic and diabetic kidney disease. We evaluated the potential role of the ACE/ID polymorphism on the antiproteinuric responsiveness to ACE inhibition in NIDDM patients with nephropathy. METHODS: 35 NIDDM patients with overt proteinuria were included in this study. DNA amplified by PCR techniques was used to detect the two alleles of the ID polymorphism. Subjects were classified as II+ID group and DD group according to the presence (I) or absence (D) of a 270 base pair insertion. Ramipril was used for ACE inhibition. At a baseline and an end of the study(6 months later from baseline), arterial blood pressure, HbA1c, serum creatinine, creatinine clearance, and 24 hour urine protein amount were measured. The significant response to ACE inhibition was defined as a decline in proteinuria > or =30% of baseline. RESULTS: The MABP was decreased significantly in each groups, but the degree of BP reduction was not different between the groups. Twenty-four hour urine protein amount and creatinine clearance was not different in each groups and between CONCLUSION: Antiproteinuric effect of ACE inhibition was not associated with ACE/ID polymorphism in diabetic patients with nephropathy.