Figure 3.

Main effects of oxidized lipids and lipoproteins in chronic kidney disease (CKD). CKD is associated with increased oxidative stress, which promotes covalent modifications of lipids and lipoproteins. Lipid products of this unbalanced metabolism are oxidized phospholipids (oxPLs), fatty acid peroxidation products (FAPPs), oxysterols and F2-isoprostanes. Posttranslational modification derived products (PTMDPs) are the result of an enhanced myeloperoxidase (MPO) activity in CKD, an increased carbamylation and a massive production of advanced glycation end products (AGEs) and advanced lipoxidation end products (ALEs). ALEs are derived from lipid aldehydes issued from peroxidation of fatty acids (FAPPs). MPO catalyzes the nitrosilation on phospholipids to create oxPLs (❶). MPO are also involved in carbamylation process by the addition of thiocyanate on proteic residues (❷). Lipoproteins are also modified in CKD. First, triglyceride-rich lipoproteins (TGRL) have an impaired metabolism leading to their accumulation. Low-density lipoproteins (LDL) exhibit large amount of toxic oxidized (oxLDL) and carbamylated (cLDL) forms in CKD. These modifications lead to impaired functions and promote the progression of cardiovascular disease (CVD) especially in hemodialysis (HD) patients. High density lipoproteins (HDL) are also modified in CKD. Their whole metabolism is impaired and this dysregulation leads to many pro-atherosclerotic effects. MPO and carbamylation are greatly responsible for lipoproteins’ modifications and dysfunctions (❸) so are FAPP products that generate ALEs, especially on apolipoproteins A and B (ApoB) (❹). Abbreviations: refer to abbreviation section.