Deletion polymorphism in angiotensin-converting enzyme gene associated with parental history of myocardial infarction

doi:10.1016/0140-6736(93)91075-W

The Lancet

Volume 341, Issue 8851, 17 April 1993, Pages 991-992

https://doi.org/10.1016/0140-6736(93)91075-W Get rights and content

Abstract

In a European study an insertion (/)/deletion (D) polymorphism in the angiotensin converting enzyme (ACE) gene has been shown to be associated with the risk of myocardial infarction (Ml). In the same study, we investigated the association of the polymorphism with a parental history of fatal MI. There was an excess of both DD (odds ratio 2·6, p=0·02) and ID (odds ratio=1·9, p=0·08) genotypes among those having a parental history of Ml, confirming that genetic variation in the ACE locus could be involved in the risk of MI.

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Citation Excerpt :
DNA was extracted by the phenol chloroform method and was stored at −20 °C. ACE I/D genotypes were determined by the polymerase chain reaction using allele specific primers method as reported earlier [22]. The sense oligonucleotide primer was 5′-CTG GAG ACC ACT CCC ATC CTT TCT-3′ and the antisense primer was 5′-GAT GTG GCC ATC ACA TTC GTC AGA-3′.
To examine the association with renal damage in patients with posterior urethral valves (PUV) of two renin–angiotensin system gene polymorphisms: angiotensin converting enzyme insertion/deletion (ACE I/D) and angiotensin type 2 receptor (AT2R A1332G),
In 120 patients with PUV, after stabilization, transurethral fulguration or a Blocksom vesicostomy was performed. Records were reviewed for age at diagnosis, biochemical renal function at diagnosis, results of urine cultures, voiding cystourethrograms, radiologic, sonographic and nuclear medicine scan findings, and follow-up data. ACE I/D genotypes were determined by the polymerase chain reaction using allele specific primers.
The frequency of the ACE DD genotype was significantly higher in patients with chronic kidney disease (P = 0.02) and renal scarring (P = 0.05). These genotypes were also associated with a statistically higher incidence of vesicoureteral reflux, diurnal incontinence, proteinuria and hypertension. A significantly higher frequency of the AT2R GG genotype was found in PUV patients as compared to healthy unrelated control subjects (P = 0.001), and in PUV patients with scarring (P = 0.02).
The ACE DD and AT2R GG genotypes are associated with chronic kidney disease and scarring in PUV patients. The GG genotype incidence is higher among PUV patients compared to the control population, and further studies in this area may help understanding of the genetic basis of PUV.
Angiotensin-converting enzyme gene polymorphism in North-west Indian children with posterior urethral valves
2007, Journal of Pediatric Urology
Citation Excerpt :
DNA was extracted by the phenol chloroform method [11]. ACE I/D genotype was determined by the PCR-restriction fragment length polymorphism method of Tiret et al. [12]. The sense oligonucleotide primer was 5′-CTG GAG ACC ACT CCC ATC CTT TCT-3′ and the antisense primer was 5′-GAT GTG GCC ATC ACA TTC GTC AGA-3′.
To investigate the association of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and other risk factors with renal scarring in patients with posterior urethral valves (PUV).
Forty consecutive patients from North-west India were treated for PUV in 1997–2004. The patients were divided into group 1 (no renal scarring, n = 12) and group 2 (renal scars present, n = 28) based on dimercato-succinic acid scans. ACE I/D polymorphism was determined by polymerase chain reaction in PUV patients and unrelated healthy controls (n = 100).
Mean age at presentation was 23.7 ± 37.2 months and mean follow up was 4.8 ± 1.5 years. Preoperative mean serum creatinine levels for group 1 (non-scarred) and group 2 (scarred) were 1.1 ± 1.6 mg/dl and 1.7 ± 1.6 mg/dl, respectively. One year after treatment, the serum creatinine levels had decreased to 0.6 ± 0.1 mg/dl and 0.8 ± 0.3 mg/dl in group 1 and group 2, respectively. ACE genotype distribution in children with PUV was no different from that of controls. The occurrence of D allele was significantly (p = 0.04) higher in patients of group 2. Multivariate logistic regression analysis showed that D allele had a significant impact on renal scar formation, introducing a 4.6-fold risk (odds ratio 4.6, 95% confidence interval 1.03–20.38, p = 0.04). A highly significant correlation between the occurrence of renal scarring and presence of breakthrough urinary tract infection (odds ratio = 7.5, 95% confidence interval 1.60–35.07, p = 0.006) and serum creatinine at follow up (odds ratio = 0.6, 95% confidence interval 0.47–0.81, p = 0.03) was observed. The mean values for glomerular filtration rate (GFR) after 1 year of treatment (p = 0.006) and at follow up (p = 0.027) were significantly different between the patients with II genotype and ID/DD genotype. Hypertension was observed in 13 patients and proteinuria in nine patients with no significant difference between the patients having II/I D/DD genotypes.
The presence of D allele is associated with progression of renal scarring and reduced GFR in PUV patients.
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SHORT REPORTSDeletion polymorphism in angiotensin-converting enzyme gene associated with parental history of myocardial infarction

Abstract

J Biol Chem

Deletion polymorphism in the gene for angiotensin-converting enzyme is a potent risk factor for myocardial infarction

Nature

Familial resemblance of plasma angiotensin-converting enzyme level: the Nancy study

Am J Hum Genet

SHORT REPORTS
Deletion polymorphism in angiotensin-converting enzyme gene associated with parental history of myocardial infarction