POLYMORPHISM OF ANGIOTENSIN I CONVERTING ENZYME BECOMES AN INNATE PROPERTY IN RENAL FAILURE (original) (raw)
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Angiotensin 1 Converting Enzyme Encoding Gene Polymorphism in Renal Patients
Pakistan Journal of Medical and Health Sciences
Background: Angiotensin I is converted to angiotensin II by an angiotensin-converting enzyme, which is an important component of renin-angiotensin framework. Multifactorial chronic kidney disease includes risk factors such as hypertension, obesity, inherited factors, and diabetes. A genetic factor associated with premature signs of renal failure is predominantly increased arterial hypertension and albumin excretion, which add to the pathophysiological movement of disintegration in renal capacity. This enzymatic assay aimed to detect ACE levels in various renal patients compared with controls to confirm the relationship between ACE quality polymorphism and enzymatic ACE levels. Materials and Methods: The study population of our study included 56 patients with chronic kidney disease. Who was confirmed to have chronic kidney disease after being diagnosed in the dialysis ward of the tertiary care hospital. Results: A total of 56 chronic kidney disease were enrolled. Mean age of patients...
2018
Published by Oriental Scientific Publishing Company © 2018 This is an Open Access article licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (https://creativecommons.org/licenses/by-nc-sa/4.0/ ), which permits unrestricted Non Commercial use, distribution and reproduction in any medium, provided the original work is properly cited. Evaluation of G2350A Polymorphism of the AngiotensinConverting Enzyme (ACE) Gene in Chronic Kidney Disease
Journal of the Renin-Angiotensin-Aldosterone System, 2011
Introduction: Insertion/deletion (I/D) polymorphisms found in the angiotensin converting enzyme (ACE) gene have been associated with hypertension, diabetes and renal disease. The present study sought to determine the association of I/D polymorphisms of the ACE gene with end-stage renal disease (ESRD) patients in Malaysia. Materials and methods: A total of 380 subjects were recruited to determine the genotypes of I/D polymorphisms of the ACE gene. Genotyping was performed using a PCR method. Statistical analyses were carried out using statistical software, and a level of p < 0.05 was considered statistically significant. Results: The frequencies for II, ID and DD genotypes of the ACE gene were 24.7%, 65.80% and 9.47%, respectively, in ESRD patients, and in control subjects were 45.26%, 47.37% and 7.37% respectively. The frequency for the D allele was found to be higher (42.40%) in ESRD patients compared to control subjects (31.05%). The genotypic and allelic frequencies of I/D polymorphisms of the ACE gene differed significantly (p < 0.05) between ESRD patients and control subjects in the Malaysian population. Conclusion: The findings of this study indicate that I/D polymorphisms of the ACE gene are a useful marker and are likely to play a major role in determining genetic susceptibility to ESRD in the Malaysian population.
International Journal of Cardiology, 1996
Renal failure or kidney failure is a situation in which the kidneys fail to function adequately. Angiotensin converting enzyme plays a pivotal role in blood pressure regulation and electrolyte balance by hydrolyzing angiotensin I to angiotensin II. The Angiotensin Converting Enzyme (ACE) gene contains a polymorphism which is believed to be associated with the interpersonal variability of ACE levels in circulating blood. Elevated angiotensin II level makes deleterious effects on renal hemodynamics and induces the expression of other growth factors, leading to glomerulosclerosis. This paper attempts to find the association of ACE polymorphism with renal failure using Random Amplification of Polymorphic DNA technique arriving to the major conclusion that ACE polymorphism is an innate property in End Stage Renal Failure (ESRF) and ACE screening would be a valuable diagnostic tool in screening clinical ESRF.
Medicinski podmladak
Since the renin-angiotensin-aldosterone system (RAAS) was originally described, it has become one of the best described hormonal systems, especially regarding the fact that it plays an important role in regulating blood volume and systemic vascular resistance, and thus indirectly influencing blood pressure (BP). On the other hand, arterial hypertension is one of the most pertinent disorders which plays an important role, not only in the progression of renal failure, but also represents a risk factor for the occurrence of end stage renal disease. Several epidemiological studies pointed out the fact that genetic predisposition accounts for about 30% of the BP variability. Up to date, there are several RAAS genes that may have effect in long-term BP control, but ACE is the most important and the most thoroughly examined. In this review, we present available data regarding the influence of gene polymorphisms of ACE on its function, within the RAAS related BP regulation. Therefore, by specially describing all its potential physiological roles, it will likely offer a new insight in the renal regulation of the BP, along with its other, not less important, roles.
Biomedical Research and Therapy
Background: Chronic Kidney Disease (CKD) is progressive kidney damage in which the glomerular filtration rate (GFR) decreases by 15% of that performed by normal kidneys, with the result that the kidneys are no longer to function effectively and this condition is treated with either kidney transplantation or dialysis. Hemodialysis (HD) is a process in which the blood passes through a machine (dialyzer) to remove waste. Angiotensin Converting Enzyme (ACE) is one of the major components of the renin-angiotensin aldosterone system (RAAS) that is responsible for blood pressure regulation. Insertion/Deletion I/D polymorphism of a 287 bp Alu repeat sequence in introns 16 of the ACE gene results in three genotypes I/D, D/D and I/I. The aims of this study were to evaluate ACE genotypes and allele frequency among HD patients and control subjects and to examine the association between ACE genotypes with HD risk. Methods: A retrospective case-control study included 186 subjects, 86 HD patients ...
Background: Hypertension is one of the important contributing factors linked with both causation and development of kidney disease. It is a multifactorial, polygenic, and complex disorder due to interaction of several risk genes with environmental factors. The present study was aimed to explore genetic polymorphism in ACE-1 gene as a risk factor for CKD among hypertensive patients. Methods: Three hundred patients were enrolled in the study. Ninety were hypertensive patients with CKD taken as cases, whereas 210 hypertensive patients without CKD were taken as controls. Demographic data including age, sex, Body mass index (BMI), and other risk factors were also recorded. DNA was extracted from blood by salting out method. Genotyping of ACE gene was done by PCR technique. All the statistical analysis was done by using Epi Info and SPSS version 16 software (SPSS Inc., Chicago, IL). Results: Mean age was higher in the control group (p < 0.05). Variables among two groups were compared out of which age, BMI, hemoglobin (Hb) was found to be statistically significant whereas other variables like systolic blood pressure, trigly-ceride and low-density lipoprotein were not. Blood urea and serum creatinine levels were statistically significant in the two genotypes (p < 0.05). Total and HDL cholesterol were statistically significant for DD genotype of ACE gene (OR ¼ 1.42, 95% CI ¼ 0.72–2.81). Similarly, the risk for CKD among hypertensive patients was also associated with D allele of ACE gene (OR ¼ 1.25, 95% CI ¼ 0.86–1.79). Conclusion: It is concluded that ACE-DD genotype may be a risk factor for the causation and development of chronic kidney failure among hypertensive patients.
Nephrology Dialysis Transplantation, 1998
Introduction Background. The influence of angiotensin converting enzyme (ACE) gene polymorphism on the progression The metalloproteinase angiotensin converting enzyme of primary IgA nephropathy (pIgAN) is still debated. (ACE), which is widely distributed in tissues, hydro-Even though the allele frequency was reported to be lyses angiotensin I into angiotensin II, leading to the similar to controls, in some studies D/D patients had formation of the active molecule. This enzyme is also a faster decline of renal function and need of dialysis. able to inactivate bradykinin, a potent vasodilator [1]. Since Henoch-Schoenlein purpura (HSP) nephritis is Although significant ACE activity is found in plasma, considered a systemic vasculitis with renal lesions the majority of the enzyme is bound to the tissues, indistinguishable from pIgAN, we investigated the mostly to the vascular endothelia [2]. Plasma and effect of the ACE polymorphism on presentation and tissue ACE contents vary in the populations. Rigat progression of HSP IgAN. et al. [3] demonstrated that polymorphism in intron Methods. We examined the insertion (I) and deletion 16 of the ACE gene, identified by the insertion (I) or (D) polymorphism in intron 16 of ACE gene by PCR the deletion (D) of a 287 bp region of DNA, accounted amplification of genomic DNA of 82 patients (37 for half the variance of serum enzyme levels. children), with biopsy-proven IgAN associated with Over the last few years a large number of studies HSP enrolled in a collaborative study. have been devoted to the investigation of whether the Results. No significant association with clinical pre-ACE polymorphism is associated to diseases expression sentation at onset or with final outcome was found and outcome. A demonstration of linkage between the (functional impairment at outcome in 31.8% D/D, ACE locus and elevated blood pressure in a rat model 27.4% I/D and 44% I/I, heavy proteinuria in 36.3% of hypertension pointed to ACE as a candidate gene D/D, 21.6% I/D, and 11.1% I/I). Patients homozygous in human hypertension [4]. for the D allele had a greater number of extrarenal The D/D genotype was also found to be a genetic relapses (P=0.0028). No association was found marker associated with an elevated risk of left ventricubetween the ACE genotype and the presence of hyperlar hypertrophy in middle-aged men [5], but in protension at onset and at the end of the follow-up. No spective studies on a large number of subjects this difference was found between adults and children. association was not confirmed [6,7]. Conclusions. In this cohort of HSP IgAN, no ACE In several clinical settings the D allele was a strong I/D polymorphisms were found to be associated with and independent risk factor for coronary heart disease progressive deterioration of renal function. Different as in non-insulin dependent diabetes mellitus patients, genes possibly involved in vasculitis might more strictly independently from hypertension and lipid values [8]. modulate expression and evolution of HSP IgAN. A progressively increasing relative risk was observed in individuals heterozygous and homozygous for the Key words: ACE; DNA polymorphism; Henoch-D allele, suggesting a codominant effect. Schoenlein purpura, PCR The effects of ACE genotype and ACE activity are probably mediated by an increased generation of angiotensin II, a well known pressor hormone which acts as growth factor and matrix producer on vascular Correspondence and offprint requests to: Prof. Antonio Amoroso, smooth-muscle cells. Indeed rats transfected with ACE