Abstract
Studies concerning the role of arachidonic acid (AA) and its metabolites in kidney disease are scarce, and this applies in particular to idiopathic nephrotic syndrome (INS). INS is one of the most frequent glomerular diseases in childhood; it is characterized by T-lymphocyte dysfunction, alterations of pro- and anti-coagulant factor levels, and increased platelet count and aggregation, leading to thrombophilia. AA and its metabolites are involved in several biological processes. Herein, we describe the main fields where they may play a significant role, particularly as it pertains to their effects on the kidney and the mechanisms underlying INS. AA and its metabolites influence cell membrane fluidity and permeability, modulate platelet activity and coagulation, regulate lymphocyte activity and inflammation, preserve the permeability of the glomerular barrier, influence podocyte physiology, and play a role in renal fibrosis. We also provide suggestions regarding dietary measures that are able to prevent an imbalance between arachidonic acid and its parental compound linoleic acid, in order to counteract the inflammatory state which characterizes numerous kidney diseases. On this basis, studies of AA in kidney disease appear as an important field to explore, with possible relevant results at the biological, dietary, and pharmacological level, in the final perspective for AA to modulate INS clinical manifestations.
Highlights
Idiopathic nephrotic syndrome (INS) is one of the most frequent glomerular diseases in childhood [1]
In patients affected by nephrotic syndrome who develop early hypertension [52], a decreased concentration of 20-HETE in the proximal tubule has been observed [53] in association with increased albumin permeability in the glomeruli, which worsens proteinuria and glomerular injury [54]; this finding supports the role of 20-HETE in preserving glomerular permeability barrier to albumin
In vitro experiments of cell cultures incubated with PUFAs showed that arachidonic acid (AA) is able to induce upregulation of the expression of TGF-β, fibronectin 1 (FN1), connective tissue growth factor (CTGF), and collagen IV, all compounds related to fibrosis [67]
Summary
Idiopathic nephrotic syndrome (INS) is one of the most frequent glomerular diseases in childhood [1] It is characterized by proteinuria, caused by podocyte damage, hypoalbuminemia, hyperlipidemia, and edema [1]. No limit was given regarding the date of publication of the articles, and the following keywords were used: arachidonic acid, arachidonic acid metabolism, cell membrane, immune system, nephrotic syndrome, membrane receptor, coagulation, platelets, arachidonic acid pathway, TXA2 , LTB4 , PGE2 , CNI pharmacogesaturated fatty acid, monounsaturated fatty acids, and total omega-3 levels in human subjects. It was recently described that erythrocyte membranes of patients with INS differ from those of normal due to reduced membrane fluidity [11]
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