Abstract
Precise characterization of clinical phenotypes and revelation of genetic markers for the predisposing to have renal maladies or alter its course has been bothersome and exhausting. However, some genetic variants have been linked to kidney disorders. Methods: This study involved 120 subjects (70 Hemodialysis-treated patients with chronic renal failure and 50 healthy subjects as control). Serum biochemical parameters Creatinine, and Urea were detected as diagnostic markers to renal functions. Sixty subjects (44 patients & 16 control) were genotyped for polymorphism of the enzyme gene conversion of angiotensin. The distribution of genotype and allele frequencies for ACE-D / I SNP polymorphism has been evaluated in both groups. Results : The levels of Biochemical parameters Creatinine, and Urea in renal failure patients increased significantly when compared with healthy .The ACE genotypes distribution between subjects groups in Thi-Qar indicated that The percentage of DD genotype was found to be high in the group of patients 23 (52.3%), followed by ID 16 (36.3%) and II genotype 5 (11.4%). As, the genetic pattern in the control group showed that the genotype DD and ID patterns had the same percentage of 37.3%, followed by genotype II, 25% . Also, there is an increase of D-allele frequencies in the group of patients equivalent with healthy controls.
Highlights
Genetic factor plays an important role in chronic kidney disease progression and end—stage kidney disease (ESRD) development [1]
Angiotensin-converting enzyme (ACE) gene has in excess of 160 gene polymorphisms; Single nucleotide polymorphism (SNP) is the vast majority
There are significant differences between control groups and patients in II genotypes and the frequency of DD, but there are no significant statistical differences between them in the genotype of ID SNP ACE genotypes. These results are in accordance with a few studies, such as the Sabbar's et al [6] study in Iraq, that showed that the DD genotype percentages were identified to be 56 % high in the group of patients, led by ID 28 percent and II genotype 16 percent. They indicated significant differences in DD (P value was 0.0019 and odd ratio 2.47) between patients and control group, whereas II genotype (P value 0.02 and odd ratio 0.44) did not show a significant difference in the ID genotype (P value > 0.05), according to the results of Ali et al [15] who stated that the D allele repetition in ESRD patients was higher (42.40%) than in healthy control patients in Malaysia (31.05%)
Summary
Genetic factor plays an important role in chronic kidney disease progression and end—stage kidney disease (ESRD) development [1]. Developments in new molecular genetic techniques have presented visions in the role of genetic change in kidney disorders with the possibility of developing the path of kidney disease and benefit from precautionary treatment [2]. To order to understand the role of genetic factors to renal disorder, it is important to recognize between these possible mechanisms [3]. ACE gene has in excess of 160 gene polymorphisms; Single nucleotide polymorphism (SNP) is the vast majority. In this gene, the SNP includes either a deletion (D) allele or an insertion (1) allele in a DNA sequence of 287-basepair in intron 16 of the ACE gene coding structuring three probable genotypes: DD, 11 or ID [4]. Many studies were carried out to determine the association between ACE polymorphism and renal failure progression [4,5,6]
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