Uraemia in chronic kidney disease leads to structural modifications of lipoproteins that promote atherogenesis and cardiovascular disease, highlighting the need for novel therapeutic agents.
This review highlights the mechanisms of uraemic dyslipidaemia and emphasizes the need for novel therapeutic agents to prevent adverse lipoprotein remodelling in patients with chronic kidney disease.
Chronic kidney disease (CKD) is associated with high cardiovascular risk. CKD patients exhibit a specific lipoprotein pattern termed 'uraemic dyslipidaemia', which is characterized by rather normal low-density lipoprotein cholesterol, low high-density lipoprotein cholesterol, and high triglyceride plasma levels. All three lipoprotein classes are involved in the pathogenesis of CKD-associated cardiovascular diseases (CVDs). Uraemia leads to several modifications of the structure of lipoproteins such as changes of the proteome and the lipidome, post-translational protein modifications (e.g. carbamylation) and accumulation of small-molecular substances within the lipoprotein moieties, which affect their functionality. Lipoproteins from CKD patients interfere with lipid transport and promote inflammation, oxidative stress, endothelial dysfunction as well as other features of atherogenesis, thus contributing to the development of CKD-associated CVD. While, lipid-modifying therapies play an important role in the management of CKD patients, their efficacy is modulated by kidney function. Novel therapeutic agents to prevent the adverse remodelling of lipoproteins in CKD and to improve their functional properties are highly desirable and partially under development.
Speer et al. (Wed,) conducted a review in Chronic kidney disease (CKD). Uraemia in chronic kidney disease leads to structural modifications of lipoproteins that promote atherogenesis and cardiovascular disease, highlighting the need for novel therapeutic agents.