Abstract
Aim and MethodsWe investigated the association between polymorphisms of the angiotensin converting enzyme-1 (ACE-1) and angiotensin II type one receptor (AT1RA1166C) genes and the causation of renal disease in 76 advanced chronic kidney disease (CKD) pediatric patients undergoing maintenance hemodialysis (MHD) or conservative treatment (CT). Serum ACE activity and creatine kinase-MB fraction (CK-MB) were measured in all groups. Left ventricular mass index (LVMI) was calculated according to echocardiographic measurements. Seventy healthy controls were also genotyped.ResultsThe differences of D allele and DI genotype of ACE were found significant between MHD group and the controls (p = 0.0001). ACE-activity and LVMI were higher in MHD, while CK-MB was higher in CT patients than in all other groups. The combined genotype DD v/s ID+II comparison validated that DD genotype was a high risk genotype for hypertension .~89% of the DD CKD patients were found hypertensive in comparison to ~ 61% of patients of non DD genotype(p = 0.02). The MHD group showed an increased frequency of the C allele and CC genotype of the AT1RA1166C polymorphism (P = 0.0001). On multiple linear regression analysis, C-allele was independently associated with hypertension (P = 0.04).ConclusionACE DD and AT1R A/C genotypes implicated possible roles in the hypertensive state and in renal damage among children with ESRD. This result might be useful in planning therapeutic strategies for individual patients.
Highlights
Chronic kidney disease (CKD) is a complex disorder encompassing a large variety of phenotypes
angiotensin converting enzyme (ACE)-activity and Left ventricular mass index (LVMI) were higher in maintenance hemodialysis (MHD), while creatine kinase-MB fraction (CK-MB) was higher in conservative treatment (CT) patients than in all other groups
The genotypic level was visible at the allelic level as D allele was found in a higher frequency in MHD patients than in the controls. (X2 = 46.89, P = 0.0001, Odds ratios (OR) = 0.13, 95% confidence intervals (CI) = 0.07-0.24)
Summary
Chronic kidney disease (CKD) is a complex disorder encompassing a large variety of phenotypes. It has been seen that RAS blockers i.e. both angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers lower blood pressure and can attenuate or prevent renal damage [10]. Major inter-individual treatment responses to RAS inhibitors have been noted [11] and it remains difficult to predict responders based on known patho-physiological characteristics [12]. In such a situation, genetic variability in the genes of different components of RAS is likely to contribute for its heterogeneous association in the renal disease patients. The genetic polymorphisms of these key components of RAS provide a basis for studying the relationship between genetic variants and the development of vascular and/or renal damage in individual subjects [15,16]
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