Abstract
Background: Primary nephrotic syndrome (NS) is a common kidney disease in children. Objectives: The present study was aimed to investigate whether rs5370 G>T (lys198Asn) genetic variant of endothelin-1 (ET-1) is involved in the susceptibility to NS. Patients and Methods: This case-control study was performed on 138 patients with NS and 150 healthy children. Genomic DNA was extracted from whole blood using salting out method. Polymorphism of the ET-1 rs5370 G>T (lys198Asn) polymorphism detected by T-ARMS-PCR as well as PCR-RFLP method. Results: The results showed that the genotype and allelic frequencies of the ET-1 rs5370 G>T variant were not significantly different between cases and controls. Furthermore, subgroup analysis showed that rs5370 G>T variant was not associated with gender of patients. In NS patients the genotype was not associated with cholesterol, triglyceride, total protein and albumin levels. Conclusions: In conclusion, our findings indicate that ET-1 rs5370 G>T is not associated with NS. Further studies with larger sample sizes and different ethnicities are required to validate our findings.
Highlights
Primary nephrotic syndrome (NS) is a common kidney disease in children
Subgroup analysis showed that rs5370 G>T variant was not associated with gender of Endothelin-1 Gene polymorphism patients
In conclusion, our findings indicate that ET-1 rs5370 G>T is not associated with NS
Summary
Primary nephrotic syndrome (NS) is a common kidney disease in children. Objectives: The present study was aimed to investigate whether rs5370 G>T (lys198Asn) genetic variant of endothelin-1 (ET-1) is involved in the susceptibility to NS.Article history: Received: 28 August 2016 Accepted: 1 December 2016. Primary nephrotic syndrome (NS) is a common kidney disease in children. Nephrotic syndrome (NS) is a chronic pediatric disorder characterized by heavily proteinuria, hyperlipidemia, hypoalbuminemia, and peripheral edema [1,2]. It has been proposed that minimal change NS (MCNS) and focal segmental glomerulosclerosis (FSGS) are the most common causes of idiopathic NS in children [3]. ET-1 is encoded by the EDN1 gene which is located in chromosome 6 (6p21–24), and is a potent vasoconstrictor that acts as a modulator of vasomotor tone and vascular remodeling [4,5]. Transgenic animal models in which the human ET-1 gene was transferred into the germline of mice were established independently by two research groups [6,7]. The blood pressure was not affected even after the de-
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