Abstract
Kidney disease is clinically characterized by increasing rates of urinary albumin excretion, starting from normo-albuminuria, which progresses to microalbuminuria, macro albuminuria nephropathy, and eventually to end stage renal disease. This study aimed to estimate the frequencies of different polymorphisms of ACE gene in chronic kidney disease, and Healthy control. A case-control study design was carried out on 207 patients they were classified into 104 nephrotic syndrome and 103 chronic kidney injury patients in addition to 102 healthy subjects. The I/D polymorphism of the ACE gene was determined sequences of the sense and antisense primers PCR was performed in a final volume of 50 μl. Results: Genotype frequencies 2nd PCR (II, ID and DD-genotypes) in control group were found to be 12, 74 and 58; respectively while genotype frequencies 2nd PCR (II, ID and DD-genotypes) in CKD group were 0, 45 and 58; respectively. In Chronic Kidney Disease (CKD) patients, there were significant increase in [Creatinine (mg/dL), Cholesterol (mg/dL), T.G (mg/dL), LDL (mg/dL), Uric Acid (mg/dL)], 7.70 ± 2.98, 236.45 ± 42.19, 256.41 ± 43.11, 149.78 ± 12.78, 6.68 ± 0.82; respectively compared to control group (p<0.01). But there was a significant decrease in albumin 3.02 ± 0.419, compared to control group (p<0.01). From this study we conclude that there is a correlation between polymorphism of angiotensin converting enzyme gene and chronic kidney disease, especially DD genotype, which increases the chances of development to the stage of renal failure.
Highlights
Angiotensinogen is produced in the liver and is found continuously circulating in the plasma
From this study we conclude that there is a correlation between polymorphism of angiotensin converting enzyme gene and chronic kidney disease, especially DD genotype, which increases the chances of development to the stage of renal failure
Our study aims to estimate the frequencies of different polymorphisms of angiotensin converting enzyme (ACE) gene in chronic kidney disease, and Healthy control group
Summary
Angiotensinogen is produced in the liver and is found continuously circulating in the plasma. Renin acts to cleave angiotensinogen into angiotensin I. The conversion of angiotensin I to angiotensin II is catalyzed by an enzyme called angiotensin converting enzyme (ACE). After angiotensin I is converted to angiotensin II, it has effects on the kidney, adrenal cortex, arterioles, and brain by binding to angiotensin II type I (AT) and type II (AT) receptors [1]. Angiotensin converting enzyme is encoded by the ACE gene, which is found in 17q23 and encoded by a 21 kb gene that consists of 28 exons and 25 introns. Single nucleotide polymorphisms (SNPs) frequently occur in the ACE gene, it has been identified 6 polymorphism markers of ACE, and Alu insertion/deletion (I/D) fragment in the 16th intron is the most investigated, ACE gene polymorphism could be divided into DD, ID, II genotype based on this I/D polymorphic marker locus. Single nucleotide polymorphisms (SNPs) frequently occur in the ACE gene, it has been identified 6 polymorphism markers of ACE, and Alu insertion/deletion (I/D) fragment in the 16th intron is the most investigated, ACE gene polymorphism could be divided into DD, ID, II genotype based on this I/D polymorphic marker locus. (1) the I/D polymorphism is located on a non-coding region (i.e., intron) of the ACE gene, several investigators found that the D allele is related to increased activity of ACE in serum [2]
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