Polymorphic Genes for Kinin Receptors, Nephropathy and Blood Pressure in Type 2 Diabetic Patients

Abstract

Background/Aims: There is evidence that hereditary predisposition contributes to the development of diabetic nephropathy and hypertension. Polymorphisms in the genes for bradykinin receptors (B₁R and B₂R) were found to be associated with decreased risk of the development of end-stage renal disease. This study examines whether B₁R G^–699C and B₂R C¹⁸¹T polymorphisms are associated with microalbuminuria or overt nephropathy, or blood pressure variation in type 2 diabetic subjects. Methods: B₁R and B₂R polymorphisms were determined in 153 type 2 diabetic patients with microalbuminuria, 132 with overt nephropathy (macroalbuminuria or chronic renal failure), and 161 patients with normoalbuminuria despite diabetes duration longer than 10 years. Results: Distributions of the examined polymorphisms did not differ between patients with microalbuminuria or overt nephropathy, compared to normoalbuminuric control subjects. Patients carrying the B₂R T allele had lower DBP, compared with non-carriers: 83.6 ± 12.0 vs. 87.4 ± 12.1 mm Hg, p < 0.05. Among patients not receiving ACEI, both SBP and DBP was significantly lower in B₂R T allele carriers, compared to non-carriers (137.2 ± 20.3 vs. 146.5 ± 21.7 mm Hg, and 80.3 ± 11.9 vs. 85.8 ± 11.6 mm Hg, p < 0.05). Conclusions: Examined polymorphisms are not associated with the increased risk of incipient or overt nephropathy in type 2 diabetic patients. B₂R C¹⁸¹T polymorphism may contribute to blood pressure variation in these subjects.