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Médecine B, Centre Hospitalier
Universitaire, Angers, Paris, France.
Laboratoire de Biochimie B, Centre Hospitalier Universitaire, Angers,
Paris, France.
Service d'informatique Médicale,
Hôpital Broussais, Paris, France.
§
Institut National de la Recherche Médicale
(INSERM U367), Paris, France.
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Diabétologie, Endocrinologie,
Hôpital Bichat, Paris, France.
Correspondence to Dr. Michel Marre, Endocrinologie, Hôpital Bichat, 46 rue Henri Huchard, 75877 Paris Cedex 18, France. Phone: 33-0-140-257-301; Fax: 33-0-140-258-842; E-mail: michel.marre{at}bch.ap-hop-paris.fr
Abstract. Angiotensin-I converting enzyme (ACE) regulates renal
hemodynamics. Its insertion/deletion (I/D) polymorphism, which determines most
of ACE interindividual variance, was proposed as a genetic marker for diabetic
nephropathy. A substitution (M235T) polymorphism in angiotensinogen (AGT) may
interact with ACE I/D polymorphism for the risk of diabetic nephropathy, but
their prognostic values have to be established by follow-up studies. A total
of 310 type 1 diabetes mellitus patients who attended the diabetic clinic in
Angers (France) took part in a prospective, observational, follow-up study.
Glycohemoglobin, BP, plasma creatinine, and urinary albumin excretion were
determined periodically. Nephropathy was classified as absent, incipient
(microalbuminuria), established (proteinuria), advanced (plasma creatinine
150 µmol/L), and terminal (renal replacement therapy). The main end
point was the occurrence of a renal event defined as the progression to a
higher stage of diabetic nephropathy. At baseline, 251 (81%) patients had no
nephropathy, 35 (11%) had incipient nephropathy, 18 (6%) had established
nephropathy, and 6 (2%) had advanced nephropathy. The ACE I/D and M235T AGT
polymorphisms were in Hardy-Weinberg equilibrium in the patients. The median
duration of follow-up was 6 yr (range, 2 to 9 yr). The occurrence of renal
events was significantly influenced by ACE genotype (log-rank II
versus ID versus DD, P < 0.03) with a dominant
deleterious effect of the D allele: ID or DD versus II (adjusted
hazard ratio, 5.0; 95% confidence interval, 1.5 to 16.6). Other contributors
were high glycohemoglobin and systolic BP. In the patients who initially were
free of nephropathy, baseline plasma ACE concentration was higher in patients
who progressed to microalbuminuria (571 ± 231 versus 466
± 181 µg/L; P = 0.0032); the D allele independently favored
the occurrence of incipient nephropathy (adjusted hazard ratio, 4.5; 95%
confidence interval, 1.1 to 19.4); other contributors were male gender,
baseline systolic BP, and urinary albumin excretion. The AGT M235T
polymorphism was not associated with renal events. The D allele of the ACE I/D
polymorphism is an independent risk factor for both the onset and the
progression of diabetic nephropathy in type 1 diabetes mellitus patients.
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