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Diabetes 54:2961-2967, 2005
© 2005 by the American Diabetes Association, Inc.

Modulation of the Renal Response to ACE Inhibition by ACE Insertion/Deletion Polymorphism During Hyperglycemia in Normotensive, Normoalbuminuric Type 1 Diabetic Patients

Laurent Weekers1, Béatrice Bouhanick2, Samy Hadjadj3,4, Yves Gallois5, Ronen Roussel6,7, Franck Pean7, Amos Ankotche6, Gilles Chatellier8, François Alhenc-Gelas9, Pierre J. Lefebvre1, and Michel Marre6,7

1 Division of Diabetes, Nutrition, and Metabolic Disorders, Department of Medicine, Centre Hospitalier Universitaire du Sart Tilman, Liege, Belgium
2 Médecine Interne et Risque Vasculaire, Rangueil Hospital, Toulouse, France
3 Department of Endocrinology and Diabetology, University Hospital, Poitiers Cedex, France
4 Institut National de la Santé et de la Recherche Médicale (INSERM) ERM 324, University Hospital, Poitiers Cedex, France
5 Biochimie, Faculté de Médecine d’Angers, Angers Cedex, France
6 Department of Endocrinology, Diabetology and Nutrition, Bichat Hospital, Assistance Publique des Hôpitaux de Paris, Paris Cedex, France
7 INSERM U695, Université Paris VII Faculté de Médecine X Bichat, Paris, France
8 Department of Biostatistics, Georges Pompidou European Hospital, Assistance Publique des Hôpitaux de Paris, Paris, France
9 INSERM U367/652, Paris, France

ACE inhibition protects kidney function, but ACE insertion/deletion (I/D) polymorphism affects renal prognosis in type 1 diabetic patients. ACE genotype may influence the renal benefits of ACE inhibition. We studied the impact of ACE I/D polymorphism on the renal hemodynamic changes induced by ACE inhibition in type 1 diabetes. We studied renal hemodynamics (glomerular filtration rate [GFR], effective renal plasma flow [ERPF], filtration fraction [GFR/ERPF], mean arterial pressure [MAP], and total renal resistances [MAP/ERPF]) repeatedly during normoglycemia and then hyperglycemia in 12 normotensive, normoalbuminuric type 1 diabetes and the II genotype (associated with nephroprotection) versus 22 age- and sex-matched subjects with the ACE D allele after three randomly allocated 2- to 6-week periods on placebo, 1.25 mg/day ramipril, and 5 mg/day ramipril in a double-blind, cross-over study. During normoglycemia, the hemodynamic changes induced by ramipril were similar in both genotypes. During hyperglycemia, the changes induced by ramipril were accentuated in the II genotype group and attenuated dose dependently in the D allele group (treatment-genotype interaction P values for ERPF, 0.018; MAP, 0.018; and total renal resistances, 0.055). These results provide a basis to different renal responses to ACE inhibition according to ACE genotype in type 1 diabetes.

Address correspondence and reprint requests to Michel Marre, Department of Endocrinology, Diabetology and Nutrition, Bichat Hospital, Assistance Publique des Hôpitaux de Paris, 46 rue Henri Huchard, 75877 Paris Cedex 18, France. E-mail: michel.marre{at}bch.ap-hop-paris.fr

Abbreviations: ERPF, effective renal plasma flow; GFR, glomerular filtration rate; I/D, insertion/deletion; MAP, mean arterial pressure; TRR, total renal resistance; UAE, urinary albumin excretion


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Copyright © 2005 by the American Diabetes Association.