Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.44 (AGT)
 770 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the study was to determine whether DNA polymorphisms at the renin-angiotensin-aldosterone (RAS) genes were associated with evolution to renal scar formation and, consequently, with reflux nephropathy (RN) in patients with vesicoureteral reflux (VUR). Some authors have suggested that the DD genotype of the angiotensin-converting enzyme (ACE) gene would be an adverse renal prognosis factor. We recruited 246 patients (aged 3 months to 22 years) from four Spanish hospitals. These included 69 patients with VUR, 110 with RN (determined by absence/presence of renal scarring on dimercaptosuccinc acid scan), 27 with chronic renal failure due to RN, and 40 patients (control group) with urinary tract infection and normal findings on renal ultrasonography and voiding cystoureterogram. The ACE I/D, angiotensin II type 1 receptor AT1 A1166C, angiotensin II type 2 receptor A3123C AT2, and angiotensinogen AGT M235T polymorphisms were determined on the basis of polymerase chain reaction amplification. ACE serum levels were determined by spectrophotometric methods. We found no statistical differences in the distribution of RAS polymorphisms between the different groups. The ACE D allele was linked to higher ACE serum levels. We found no association between ACE I/D polymorphism and presence of hypertension, proteinuria, grade of VUR, or unilateral/bilateral VUR. Patients with the DD genotype had a lower incidence of febrile urinary tract infection as a first symptom of VUR/RN (P<0.05). We conclude that genetic polymorphisms of RAS components are not independent prognostic indicators of renal scarring in patients with VUR.
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PMID:Renin-angiotensin system polymorphisms and renal scarring. 1257 98

Polymorphisms of some genes of the renin-angiotensin system (RAS), such as angiotensinogen (AGT; M235T), angiotensin II type 2 receptor (AT2; C3123A), and angiotensin-converting enzyme (ACE; insertion/deletion (I/D)) are involved in the development and progression of coronary artery disease (CAD) in diabetic individuals. In the present study, we aimed to determine whether three polymorphisms, AGT-M235T, AT2-C3123A, and ACE I/D are associated with CAD in Saudi patients with type two diabetes mellitus (T2DM). In 266 patients with CAD (169 patients with T2DM and 97 without T2DM), restriction fragment length polymorphism analysis was used to detect polymorphisms in the three RAS genes. Within the CAD+T2DM group, for the ACE gene (I/D), homozygous DD was found in 65.68%, 25.44% carried the heterozygous ID, and 8.88% carried the homozygous II. Within the CAD-T2DM group, DD was found in 55.67%, 26.8% carried the ID, and 17.53% carried the II. The odds ratio (OR) of the ACE ID+DD vs. II was 2.18, with a 95% confidence interval (CI) of 1.04-4.60, and P = 0.04. Thus, we found an association between the ACE DD polymorphism and CAD in Saudi patients with T2DM, but not between the AT2 C3123A and AGT M235T polymorphisms and CAD.
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PMID:Renin-angiotensin system gene polymorphisms and coronary artery disease in Saudi patients with diabetes mellitus. 3196 89