Introduction: To determine the incidence of ACE I/D GENE POLYMORPHISM and It's effect on serum ACE level. Material and method: This prospective analytical study was done on 88 healthy kidney donate. The serum ACE determined by spectophotometric assay and genotype by polymerase chain reaction (PCR).Result: 88 healthy individual (70 males: %80 and 18 females: 20%) was selected for the study. Mean age for each genotype were: II=29,88 +/- 8/07, ID=31/04+/- 7/06, DD=29/29+/- 6/82. The frequency of deletion and insertion alleles were 0/48 and 0/51 respectively. Mean serum ACE +/- SD in each genotype were II=32/06+/- 24/2, ID=36/25 +/- 20/87, DD=50/68+/- 24/59.Conclusion: In this study we show the effect of ACE I/D GENE POLYMORPHISM on the serum ACE level in Iranian people. Frequency of I,D alleles were 51/15% and 48/85% respectively. The mean of serum ACE level in each genotype was lower in female than male but due to small number of females documentation with greater number of cases is recommended. This is the first description of ACE GENE POLYMORPHISM in Iranian population which can be used as a pilot for future steadies.

It has recently been shown that an insertion (I)/deletion (D) POLYMORPHISM exists in the angiotensin-converting enzyme (ACE) GENE that can affect the serum ACE level. There are three genotypes: DD, DI, and II, with the ACE level being highest in DD, intermediate in DI, and lowest in II. The DD genotype has been reported as a GENEtic risk factor for diabetes mellitus. In the present investigation, 170 patients with type 2 diabetes mellitus (T2DM) and 144 control subjects were studied.The ACE I/D POLYMORPHISM was determined by polymerase chain reaction (PCR) utilizing specific primers. ACE activity was determined spectrophotometrically. Distributions of ACE GENE (I/D) POLYMORPHISM and allele frequencies in patients with T2DM were significantly different from those in control (P < 0.001); D allele frequency was 51% in T2DM vs. 48% in controls. The level of ACE activity was significantly higher in the DD genotype (91.1±23.18) than those in ID (60.6±22.8) and in II genotypes (36.8±6.9). There was a significant difference in genotype distribution between the two groups (P < 0.001). New normal ranges of serum ACE level were determined for each genotype.Moreover, we found test sensitivity to be 62.3%. Serum ACE activity was significantly associated with ACE (I/D) GENE POLYMORPHISM.

Angiotensin I-converting Enzyme (ACE) GENE POLYMORPHISM; genotype DD or D allele may be involved with an increased susceptibility to type 2 diabetes and diabetic nephropathy (DN). We examined the frequency of ACE GENE POLYMORPHISM in 170 patients (85 type 2 diabetes with nephropathy and 85 without it) in Tehran, Iran. DNA was extracted from the white blood cells and the I/D POLYMORPHISM of the ACE GENE was detected by PCR. The frequency of DD, ID and II genotypes in type 2 diabetic patients were 20%, 61.2% and 18.8%, and in patients with nephropathy 30.6%, 55.3%, 14.1%, respectively. The DD genotype of the DN group was higher than that of the type 2 diabetes patients (30.6% vs 20%, P=0.157, RR=1.3) and the control group (30.6% vs 14.3%, P=0.006, RR=2.9). The frequency of D allele in nephropathic patients was 58.2% as compared to the type 2 diabetic patients without nephropathy (50.5%) P=0.19, RR=1.16. The D allele frequency in the DN group was found slightly higher than of the type 2 diabetes (X2=0.684, OR=0.709, 95%CI: 0.313-1.606, P=0.408) which indicated the D allele was not associated with DN. It is suggested that DD genotype and D allele are not associated with diabetic nephropathy.      

Introduction: Angiotensin converting enzyme (ACE) is an exopeptidase that converts Angiotensin I to Angiotensin II. Angiotensin II is a potent vasoconstrictor and releases aldosterone, and have a critical role in hypertension. In this study, ACE insertion / deletion (I/D) POLYMORPHISM and ACE activity was determined in patients with coronary artery disease (CAD) and normal subjects. The correlation of these parameters with important CAD risk factors were also evaluated.Methods: 204 subjects were assigned to patients and normal groups based on their angiography results. Serum ACE activities were assayed by HPLC and I/D POLYMORPHISM were analyzed by PCR method. Important risk factors such as diabetes mellitus, hypertension, lipid profiles, ejection fraction, smoking and opium consumption were also recorded. Results: CAD was higher in DD genotype subjects (OR= 2.45; CI= 1.05-5.73), and ACE activity was about twice in DD compared to II genotypes. ACE activity was higher in hypertensives and diabetics in CAD group (p<0.001), but in the normal group it did not have any correlation with these risk factors. The rate of opium use was higher in ID and DD subjects.Conclusion: DD genotype is a risk factor for CAD and ACE activity is higher in this genotype. However, there is not any correlation between ACE activity and CAD.

Introduction. The kidney is the main source of serum Klotho production. Immunosuppressive agents could affect the kidney in this regard. The effect of the ACE GENE POLYMORPHISM on Klotho production is a less studied area. This study aimed to assess serum Klotho and ACE GENE in a group of stable kidney transplant recipients. Materials and Methods. In a cross-sectional study, 30 kidney transplant recipients with stable allograft function and 27 healthy young individuals were assessed for their serum Klotho levels. The ACE GENE POLYMORPHISMs were studied in both groups. Results. Klotho level was higher in kidney transplant recipients than the controls, but the difference was not significant (2. 76 ± 2. 41 ng/mL versus 2. 01 ± 1. 41 ng/mL, respectively). In both groups, serum Klotho level was higher in those with the I>I POLYMORPHISM, the men, those with higher glomerular filtration rate, and younger individuals, but the differences did not reach a significant level. Higher body mass index was significantly associated with lower serum Klotho level in both groups. Conclusions. Klotho level after kidney transplantation meets the range in healthy individuals, and it is not affected by the ACE GENE POLYMORPHISM.