Angiotensin-Converting Enzyme Gene Deletion Polymorphism

Markus, H.S.; Barley, J; Lunt, Ross; Jm, Bland; Jeffery, Steve; Carter, ND; Brown, Martin M.

doi:10.1161/01.str.26.8.1329

Cited by 157 publications

(33 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…No difference was found in the ACE I/D genotype distributions in subgroups with or without coronary artery disease, hypertension, left ventricular hypertrophy, and chronic cardiac failure (table 4). These findings are in agreement with previous data [16], but in contrast to those reported in other settings [8, 9, 10]. However, in uremics other risk factors may account for inconsistencies.…”

Section: Discussionsupporting

confidence: 93%

“…It was also suggested to contribute to end-stage renal disease (ESRD) in individuals with higher circulating ACE levels. On the other hand, the DD genotype has been associated with myocardial infarction [7], stroke [8], hypertrophic cardiomyopathy [9], cardiac hypertrophy [10], and idiopathic or ischemic dilated cardiomyopathy [11]. Finally, in essential hypertension, the DD genotype has been suggested as a risk factor for the development of organ damage [12].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Polymorphism of the Angiotensin-Converting Enzyme Gene in End-Stage Renal Failure Patients

Aucella

Vigilante

Margaglione

et al. 2000

Nephron

View full text Add to dashboard Cite

The plasma levels of angiotensin-converting enzyme (ACE) are modulated by the insertion (I)/deletion (D) polymorphism within the ACE gene locus. An association between progressive renal disease, raised cardiovascular risk, and ACE plasma levels has been shown. To evaluate the genotype frequencies of the I/D polymorphism in terminal renal failure, we have enrolled 341 dialysis patients (321 on hemodialysis and 20 on peritoneal dialysis) in a district of southern Italy (Foggia). As controls, 1,307 subjects from the same area have been enrolled. Genomic DNA was obtained from leukocytes, and the ACE I/D polymorphism was determined by polymerase chain reaction. Among uremics, 151 subjects (44.3%) carried the DD genotype, 149 (43.7%) the ID, and 41 (12.0%) the II genotype. In controls, 560 subjects (42.8%) had the DD genotype, 577 (44.1%) the ID, and 170 (13.1%) the II genotype (p = n.s.). Among patients, the frequency of DD subjects was higher in men (48.3%) than in women (39.7%, p < 0.01). A slight different frequency of the DD genotype was found according to the duration of dialysis treatment: 47.5% in patients on dialysis up to 60 months and 41.7 and 40.6% in those with a dialytic age of 60–120 and >120 months, respectively (p for trend: 0.53). Patients with or without cardiovascular diseases, such as hypertension, left ventricular hypertrophy, coronary artery disease, and chronic cardiac failure, did not exhibit any difference in ACE I/D allele and genotype frequencies (p always >0.05). In conclusion, frequencies of the ACE DD genotype were similar in uremics and in controls and did not differ between patients with and without cardiovascular diseases. A nonsignificant inverse relationship with the time spent on dialysis was observed, suggesting that ACE I/D polymorphism may influence the cardiovascular death rate.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Polymorphism of the Angiotensin-Converting Enzyme Gene in End-Stage Renal Failure Patients

Aucella

Vigilante

Margaglione

et al. 2000

Nephron

View full text Add to dashboard Cite

show abstract

“…The finding that patients with MLI have more frequently a family history of hypertension may suggest that genetic factors might be involved in favoring such a brain pathology. Recent observations, coming from molecular biology studies, suggest that a subgroup of hypertensive patients carries genetically determined abnormalities in the biological mechanisms for blood pressure regulation (angiotensin-converting enzyme gene deletion polymorphism), which may predispose to organ damage and to lacunar infarct [19]. Longitudinal studies are necessary to further elucidate these relationships.…”

Section: Discussionmentioning

confidence: 99%

Vascular Risk Factors Linked to Multiple Lacunar Infarcts

Spolveri¹,

Baruffi²,

Cappelletti³

et al. 1998

Cerebrovasc Dis

View full text Add to dashboard Cite

Background: The pathogenesis of lacunar infarcts is still incompletely established. Data from the literature suggest that vascular risk factors differ among patients with multiple (MLI) and single lacunar infarcts (SLI). We reexamined this hypothesis using stricter inclusion criteria and a less selected study population. Methods: We evaluated 136 patients consecutively admitted for first-ever minor stroke to a general hospital with the characteristics of a community hospital. Vascular risk factors were studied by univariate and multivariate statistical analyses among the following subgroups of patients, classified according to CT findings: (a) with lacunar infarct; (b) with nonlacunar infarct (NLI); (c) with SLI; (d) with MLI; (e) with single, either lacunar or nonlacunar, infarct. Results: No significant difference was observed between patients with lacunar infarcts and patients with NLI. Compared to patients with SLI or NLI, patients with MLI had significantly more often a family history of hypertension, cardiomegaly on the chest radiograph and CT leukoaraiosis as well as a higher systolic and diastolic blood pressure on admission. Logistic regression analysis selected CT leukoaraiosis, Rx cardiomegaly and admission diastolic blood pressure as independent, significant predictors of MLI. Conclusion: In patients with first-ever minor stroke, the risk factor profile differs according to the evidence of SLI or MLI on the CT scan. In terms of risk factors, patients with SLI seem more similar to those with NLI than those with MLI. Based on the predicting effect of variables linked with type and severity of arterial hypertension, the CT appearance of MLI might express a more univocal and specific cerebrovascular pathology (hypertensive arteriolosclerosis).

show abstract

“…A variant form of the ACE gene, involving intronic insertion/deletion of a 287-base-pair (bp) Alu sequence, is associated with increased plasma and tissue activity of this enzyme [9]. It is considered that the ACE gene polymorphism has been implicated as a risk factor for left ventricular hypertrophy, myocardial infarction and stroke [10, 11, 12]. A variant form of the AGT gene, resulting in the substitution of threonine for methionine at position 235 (M235T), is associated with increased circulating levels of AGT.…”

Section: Introductionmentioning

confidence: 99%

Relationship between Polymorphism in the Angiotensinogen, Angiotensin-Converting Enzyme or Angiotensin II Receptor and Renal Progression in Japanese NIDDM Patients

Tomino

Makita

Shike

et al. 1999

Nephron

View full text Add to dashboard Cite

We determined the relationship between the gene polymorphism of angiotensinogen (AGT), angiotensin-converting enzyme (ACE), or angiotensin II receptor (AT1R) and the progression of diabetic nephropathy in a multicenter trial of ethnically homogeneous Japanese patients with non-insulin-dependent diabetes (NIDDM). Gene polymorphism of ACE I/D, AGT M235T and AT1R A1166C was determined by polymerase chain reaction amplification using allele-specific primers. Japanese NIDDM patients (n = 1,152) were selected from several diabetic clinics. All patients were divided into three groups as follows: (1) group I (n = 407): normoalbuminuric patients; (2) group II (n = 327): microalbuminuric patients, and (3) group III (n = 418): overt albuminuric patients. Clinical factors for investigation in all patients were the date of birth, gender, levels of urinary albumin excretion, findings of the ocular fundus, duration of diabetes, hemoglobin A1c and blood pressure. It appears that genetic polymorphisms in the renin-angiotensin systems, i.e. ACE or AT1R, may affect the progression to renal failure of patients (especially females) with NIDDM.

show abstract

Angiotensin-Converting Enzyme Gene Deletion Polymorphism

Abstract: The deletion polymorphism in the angiotensin-converting enzyme gene is a new independent risk factor for lacunar stroke but is not a risk factor for stroke associated with carotid stenosis.

Cited by 157 publications

References 13 publications

Polymorphism of the Angiotensin-Converting Enzyme Gene in End-Stage Renal Failure Patients

Polymorphism of the Angiotensin-Converting Enzyme Gene in End-Stage Renal Failure Patients

Vascular Risk Factors Linked to Multiple Lacunar Infarcts

Relationship between Polymorphism in the Angiotensinogen, Angiotensin-Converting Enzyme or Angiotensin II Receptor and Renal Progression in Japanese NIDDM Patients

Contact Info

Product

Resources

About