Abstract
Background: The most common glomerular disorder in children is nephrotic syndrome, associated with high morbidity despite notable advances in its treatment. Many of the nephrotic syndrome complications, including the increased risk of atherosclerosis and thromboembolism, can be linked to dysregulated lipid metabolism and dyslipidemia. Paraoxonase enzyme is responsible for the most of the antioxidant properties of HDL, thus preventing the formation of atherogenic ox-LDL molecules, and lecithin cholesterol acyltransferase is intimately involved in HDL maturation and is a key component of the reverse cholesterol transport pathway, which removes excess cholesterol molecules from the peripheral tissues to the liver for excretion. Objectives: The present study aimed to investigate the serum activities of paraoxonase-1 (PON-1) and lecithin cholesterol acyltransferase (LCAT) in children with nephrotic syndrome in an active phase (as newly diagnosed or old cases with acute relapse). Also, to study any correlation exists between paraoxonase-1 activity and lipid profile. Methods: This study consists of group 1 with 40 cases of nephrotic syndrome in the age group of (2-14 years) and group 2 with 40 age and sex-matched healthy controls. Lipid profile and paraoxonase activity, lecithin cholesterol acyltransferase activities were measured in both groups’ serum samples. Results: Statistical analysis of student’s t-test showed that the mean levels of total cholesterol, triglycerides, LDL were significantly increased in group 1 when compared to Group 2 (p <0.001). PON1 and lecithin cholesterol acyltransferase levels were significantly lower in group 1 compared to group 2, and there is no significant difference among nephrotic groups. Conclusions: Both paraoxonase-1 enzyme and lecithin cholesterol acyltransferase are considered good promising predictors for nephrotic syndrome and other parameters such as LDL, HDL, and TG. The significantly decreased paraoxonase-1 enzyme and lecithin cholesterol acyltransferase activities result in increased oxidation of LDL, thus accelerating atherosclerosis.
Highlights
The most common glomerular disorder in children is nephrotic syndrome (NS)
The present study aimed to investigate the serum activities of paraoxonase-1(PON-1) and lecithin cholesterol acyltransferase (LCAT) in children with nephrotic syndrome in an active phase
It catalyzes the hydrolysis of multiple compounds such as arylesterase, lactones and hydroperoxides.7Human LCAT is a glycoprotein made up of 416 amino acids circulating in plasma associated with lipids and apolipoproteins in the high-density lipoprotein (HDL).[8]
Summary
The most common glomerular disorder in children is nephrotic syndrome (NS). Nephrotic syndrome is manifested as heavy (nephrotic-range) proteinuria (>40 mg/h/m2 or >50 mg/kg/day or protein/creatinine ratio >0.2 g/mmol (>2 g/g).Many of the nephrotic syndrome complications, including the increased risk of atherosclerosis and thromboembolism, can be linked to dysregulated lipid metabolism and dyslipidemia.1The paraoxonase[1] (PON1) is a serum enzyme involved in lipid metabolism.[2,3] It is bound to high-density lipoprotein (HDL) and acts as an antioxidant for the low-density lipoproteins (LDL) by hydrolyzing lipid peroxides, preventing LDL oxidation and subsequently leading to an anti-atherogenic effect.[4,5,6]Paraoxonase 1 (PON1) is a free radical scavenging system that plays a role in detoxifying a wide range of substrates such as organophosphate compounds and carcinogenic lipidsoluble radicals from lipid peroxidation. Many of the nephrotic syndrome complications, including the increased risk of atherosclerosis and thromboembolism, can be linked to dysregulated lipid metabolism and dyslipidemia.1The paraoxonase[1] (PON1) is a serum enzyme involved in lipid metabolism.[2,3] It is bound to high-density lipoprotein (HDL) and acts as an antioxidant for the low-density lipoproteins (LDL) by hydrolyzing lipid peroxides, preventing LDL oxidation and subsequently leading to an anti-atherogenic effect.[4,5,6]. The significantly decreased Paraoxonase-1 enzyme and Lecithin Cholesterol acyltransferase activities result in increased oxidation of LDL, accelerating atherosclerosis
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