ArticleJournal of clinical and diagnostic research : JCDR2016
Paraoxonase Activity and Lipid Profile in Paediatric Nephrotic Syndrome: A Cross-sectional Study.
Article in Journal of clinical and diagnostic research : JCDR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 3 citations in OpenAlex.
- Prophylactic consequences of sodium salicylate nanoparticles in cisplatin-mediated hepatotoxicity.Scientific reports · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionDyslipidaemia of Nephrotic Syndrome (NS) is known to be linked to oxidative reactions and atherosclerosis. Paraoxonase (PON1) has been implicated in the prevention of Low Density Lipoprotein (LDL) lipid peroxidation and also degrades biologically active oxidised lipids in lipoprotein.
aimThe present study was taken up to assess PON1 levels in paediatric nephrotic syndrome and also to see if any correlation exists between lipid parameters and PON1. MATERIALS AND
methodsThis study consists of Group 1 with 40 cases of NS in the age group of 2-14 years and Group 2 with 40 age and sex matched healthy controls. Lipid profile and paraoxonase activity was measured in serum samples of both the groups.
resultsStatistical analysis by student's t-test showed that the mean levels of Total Cholesterol, Trigylycerides, LDL, and VLDL were significantly increased in Group 1 when compared to Group 2 (p <0.001). The mean levels of HDL were similar in both groups. The levels of PON1 were significantly lowered in Group 1 when compared to Group 2. Correlation studies showed no significant correlation between lipid profile and PON1.
conclusionCases have atherosclerotic dyslipidaemia and significantly decreased PON1 activity. Decreased PON1 may lead to increased oxidation of LDL accelerating the process of atherosclerosis.
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