Contribution of genetic polymorphism in the renin-angiotensin system to the development of renal complications in insulin-dependent diabetes: Genetique de la Nephropathie Diabetique (GENEDIAB) study group.

Marre, Michel; Jeunemaı̂tre, Xavier; Gallois, Yves; Rodier, M.; Châtellier, Gilles; Sert, Caroline; Dusselier, L.; Kahal, Z; Chaillous, Lucy; Halimi, Serge; Müller, Andrea; Sackmann, H.; Bauduceau, B.; Bled, F.; Passa, P; Alhenc-Gelas, F

doi:10.1172/jci119321

Cited by 303 publications

(198 citation statements)

References 69 publications

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“…Evidence was found that inter-individual variation in the RAS genes contributes to a hypertension risk. Marre et al (1997) studied the contribution of genetic polymorphism in RAS to the development of renal complications in insulin-dependent diabetes in a European population.…”

Section: Discussionmentioning

confidence: 99%

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

et al. 2007

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Metabolic Syndrome (MS) is recognized as a cluster of cardiovascular risk factors. All components of MS have a genetic base. Genes of the renin angiotensin system are potential candidate genes for MS. We investigated whether angiotensin converting enzyme (ACE) gene polymorphism increases susceptibility to MS as an entity in a Mexican population. In a cross-sectional study, 514 individuals were studied including 245 patients with MS and 269 subjects without MS criteria. ACE gene polymorphism was detected using PCR. MS was defined according to The National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) criteria, except that the raised fasting plasma glucose ≥ 100 mg/dl criterion for identification of intolerance fasting glucose was modified in accordance with the suggestion of the American Diabetes Association. Patients with MS were significantly different from subjects without MS in relation to mean body mass index (BMI), waist circumference (WC), systolic blood pressure, diastolic blood pressure, glucose, total cholesterol (C), triglycerides, HDL-C, and LDL-C (P ＜ 0.0001). The differences in the mean BMI, WC, glucose, total cholesterol, triglycerides, LDL-C, and HDL-C were maintained in patients with the MS and DD genotypes (P ＜ 0.01). The DD genotype was strongly associated with MS (adjusted OR = 5.48, 95% CI 3.20-9.38, P ＜ 0.0001). We concluded that the DD genotype increases susceptibility to MS in a Mexican population. These results indicate that pharmacological and non-pharmacological treatment and a reduction in body fat will have important therapeutic implications in this disease.

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Section: Discussionmentioning

confidence: 99%

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

et al. 2007

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“…Last, ACE inhibition prevents or retards diabetic nephropathy. [11][12][13] We suggested a dominant effect of the ACE D allele on the risk of diabetic nephropathy 3 and protection with the II genotype due to low plasma ACE levels. In experimental diabetes, high blood glucose causes high intraglomerular hydraulic pressure, glomerular filtration rate (GFR), and renal plasma flow, 7 just as in type 1 diabetes.…”

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confidence: 95%

“…2,3 Family studies suggest that this may be due to differences in their genetic backgrounds. 4,5 The angiotensin I-converting enzyme (ACE) gene was tested for its association with diabetic nephropathy for several reasons.…”

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confidence: 99%

Renal Changes on Hyperglycemia and Angiotensin-Converting Enzyme in Type 1 Diabetes

Marre

Bouhanick²,

Berrut³

et al. 1999

Hypertension

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Abstract-Hyperglycemia causes capillary vasodilation and high glomerular capillary hydraulic pressure, which lead to glomerulosclerosis and hypertension in type 1 diabetic subjects. The insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene can modulate risk of nephropathy due to hyperglycemia, and the II genotype (producing low plasma ACE concentrations and probably reduced renal angiotensin II generation and kinin inactivation) may protect against diabetic nephropathy. We tested the possible interaction between ACE I/D polymorphism and uncontrolled type 1 diabetes by measuring glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) during normoglycemia (Ϸ5 mmol/L) and hyperglycemia (Ϸ15 mmol/L) in 9 normoalbuminuric, normotensive type 1 diabetic subjects with the II genotype and 18 matched controls with the ID or DD genotype. Baseline GFR (145Ϯ22 mL/min per 1.73 m 2 ) and ERPF (636Ϯ69 mL/min per 1.73 m 2 ) of II subjects declined by 8Ϯ10% and 10Ϯ9%, respectively, during hyperglycemia; whereas baseline GFR (138Ϯ16 mL/min per 1.73 m 2 ) and ERPF (607Ϯ93 mL/min per 1.73 m 2 ) increased by 4Ϯ7% and 6Ϯ11%, respectively, in ID and DD subjects (II versus ID or DD subjects: Pϭ0.0007 and Pϭ0.0005, for GFR and ERPF, respectively). The changes in renal hemodynamics of subjects carrying 1 or 2 D alleles were compatible, with a mainly preglomerular vasodilation induced by hyperglycemia, proportional to plasma ACE concentration (Pϭ0.024); this was not observed in subjects with the II genotype. Thus, type 1 diabetic individuals with the II genotype are resistant to glomerular changes induced by hyperglycemia, providing a basis for their reduced risk of nephropathy. (Hypertension. 1999;33:775-780.)

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“…7). Studies have found that the DD genotype is associated with a more rapid loss of renal function in diabetic nephropathy, 23 IgA nephropathy 24 and adult polycystic kidney disease, 25 when compared to the II or DI genotypes. The genotype does not appear to initiate or cause renal disease per se; rather it is associated with more rapid loss of renal function after disease development.…”

Section: Discussionmentioning

confidence: 99%

Loss of renal function following bone marrow transplantation: an analysis of angiotensin converting enzyme D/I polymorphism and other clinical risk factors

Juckett

Cohen

Keever-Taylor

et al. 2001

Bone Marrow Transplant

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Summary:Chronic renal failure is an acknowledged late complication of BMT. It is related to the intensive chemotherapy, radiation and supporting medications. Polymorphism in the angiotensin converting enzyme (ACE) gene is associated with progression of nephropathy caused by diabetes and IgA nephropathy. We sought to determine whether ACE genotype and other clinical factors were associated with loss of renal function after BMT. We determined the genotype of 106 adult allogeneic BMT recipients, who received a similar preparative regimen, survived 1 year, and had assessment of renal function up to 3 years after BMT. We found that the distribution of genotypes was similar to the general population; 29%, 51%, and 20% for the DD, DI, and II genotypes, respectively. There was no statistical difference in patient survival between the three groups. Among all patients, the average creatinine clearance declined from 124 (95% CI 117, 131) to 89 (95% CI 78, 100) ml/min over the 36 months after BMT. Decline in renal function over time was less for patients with the DD compared to the II genotype (P = 0.040). Renal function in patients with the DD genotype was also better than those with the DI genotype, but this was of borderline statistical significance (P = 0.055). Renal shielding reduced decline in renal function compared to no shielding (P = 0.026). We conclude that the ACE genotype does not seem to influence survival, but the DD genotype may be protective against renal injury after BMT. Furthermore, we confirm that renal shielding during TBI reduces the renal injury after BMT. Bone Marrow Transplantation (2001) The late occurrence of chronic renal failure is a known complication of allogeneic bone marrow transplantation. 1 The combined effects of intensive radiation and chemotherapy are implicated in the pathogenesis of acute and chronic renal insufficiency. Factors contributing to acute renal failure include hypotension, sepsis and the administration of nephrotoxic medications such as aminoglycoside antibiotics, cyclosporine, tacrolimus and amphotericin. A distinct syndrome of chronic renal failure after BMT termed 'bone marrow transplant nephropathy' has been described that consists of azotemia, disproportionate anemia, and hypertension. 2,3 This syndrome is thought to be due to either microvascular or renal parenchymal damage from the preparative regimen and in its most severe form resembles hemolytic uremic syndrome (HUS).Studies using animal models of BMT nephropathy have shown that angiotensin converting enzyme (ACE) inhibitors can effectively prevent and treat the syndrome. 4,5 This finding implicates the renin-angiotensin axis in the pathogenesis of the disorder. ACE is responsible for the cleavage of angiotensin I to angiotensin II, which has potent effects on vascular tone, growth and repair. The ACE gene contains a polymorphism based on the presence or absence of a 287-base pair intron. 6 The presence of the intron has been termed the 'insertion' or 'I' allele, and the absence of the intron the 'deletion' or...

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Contribution of genetic polymorphism in the renin-angiotensin system to the development of renal complications in insulin-dependent diabetes: Genetique de la Nephropathie Diabetique (GENEDIAB) study group.

Cited by 303 publications

References 69 publications

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

Renal Changes on Hyperglycemia and Angiotensin-Converting Enzyme in Type 1 Diabetes

Loss of renal function following bone marrow transplantation: an analysis of angiotensin converting enzyme D/I polymorphism and other clinical risk factors

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