Role of the deletion of polymorphism of the angiotensin converting enzyme gene in the progression and therapeutic responsiveness of IgA nephropathy.

Yoshida, Hiroaki; Mitarai, Tetsuya; Kawamura, Tetsuya; Kitajima, T; Miyazaki, Yoichi; Nagasawa, Ryo; Kawaguchi, Yoshindo; Kubo, Hitoshi; Ichikawa, Iekuni; Sakai, Osamu

doi:10.1172/jci118270

Cited by 306 publications

(185 citation statements)

References 46 publications

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“…5,6 The D allele has thereafter been associated with other CVD, including dilated and ischemic cardiomyopathy, coronary and carotid artery disease, coronary artery spasm, restenosis, left ventricular hypertrophy in hypertensives, left ventricular dysfunction, and, more recently, atherosclerotic renovascular hypertension. [7][8][9][10][11][12][13][14] However, opposite results for almost every clinical association have also been published, and therefore the value of the D/I genotyping for the purpose of cardiovascular risk stratification has been challenged [15][16][17][18][19][20][21][22][23] (for reviews, see Butler et al 24 and Agerholm-Larsen et al 25 ). Furthermore, the mechanisms by which the D allele would lead to a generalized increase in CVD risk remain largely speculative.…”

mentioning

confidence: 99%

Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction

et al. 2001

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Abstract-A deletion/insertion (D/I) polymorphism within the ACE gene may increase the risk of cardiovascular events through still unknown mechanisms. The latter may involve increased angiotensin II-induced NO breakdown and/or reduced agonist-mediated NO release. We therefore investigated whether the D allele of the ACE gene affects endothelium-dependent vasodilatation in mild-to-moderate primary hypertensive patients and healthy normotensive subjects. We compared in a cross-sectional study the forearm blood flow response of the 3 D/I genotypes with 5 incrementally increasing doses of the endothelium-dependent vasodilator acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 g ⅐ 100 mL Ϫ1 ⅐ min Ϫ1) in 142 subjects: 103 mild-to-moderate uncomplicated primary hypertensives (49.3Ϯ9.1 years old, 152Ϯ11/99Ϯ5 mm Hg) and 39 normotensives (44.6Ϯ15.3 years old, 122Ϯ12/78Ϯ6 mm Hg). We also assessed the endothelium-independent vasodilatation in the forearm, as blood flow response to 3 incrementally increasing doses of sodium nitroprusside (1, 2, and 4 g ⅐ 100 mL Ϫ1 ⅐ min Ϫ1 ). The overall genotype distribution was II, nϭ10; ID, nϭ70; and DD, nϭ62. It did not differ significantly between primary hypertensives and normotensives. A significant blunting of endothelium-dependent vasodilatation in primary hypertensive patients compared with normotensive subjects (PϽ0.001) was found. No effect of the DI genotype on endothelium-dependent and -independent vasodilatation was detected. Thus, these results obtained in a relatively large population do not support the contention that the D allele is associated with a blunting of either stimulated endothelial NO or donated NO responses in both mild-to-moderate primary hypertensive patients and normotensive subjects. (Hypertension. 2001;37:293-300.)

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confidence: 99%

Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction

et al. 2001

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“…ic variation that alters the structure, configuration, or quantity of any of the proteins involved in any of these mechanisms may contribute to interindividual variation in drug response. Early results support the notion that genetic variation may have pleiotropic effects on numerous biochemical, physiologic, and anatomic measures of response to antihypertensive drug therapy (15,17,19,(28)(29)(30)(31)(32)(33)(34)(35)(36). The RAS plays an important role in the development and extent of EH.…”

Section: Discussionmentioning

confidence: 63%

Relationship between Polymorphism of the Angiotensin-Converting Enzyme Gene and the Response to Angiotensin-Converting Enzyme Inhibition in Hypertensive Patients

2003

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“…They are intermediate in those who are heterozygous. Yoshida et al (Yoshida H 1995) later reported a greater reduction in proteinuria in response to ACE inhibition in patients with IgA nephropathy who were homozygous for the D allele. In contrast to this, other investigators have suggested a worse response to therapy in patients who carry the D allele (Parving HH 1996).…”

Section: Ace Inhibition Versus Angiotensin II (Ang Ii) Receptor Type mentioning

confidence: 99%

Diabetic Glomerulopathy

Barazi¹,

Kaur²,

Sharma³

2011

An Update on Glomerulopathies - Clinical and Treatment Aspects

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Role of the deletion of polymorphism of the angiotensin converting enzyme gene in the progression and therapeutic responsiveness of IgA nephropathy.

Cited by 306 publications

References 46 publications

Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction

Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction

Relationship between Polymorphism of the Angiotensin-Converting Enzyme Gene and the Response to Angiotensin-Converting Enzyme Inhibition in Hypertensive Patients

Diabetic Glomerulopathy

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