Abstract
The incidence of chronic kidney disease (CKD) is associated with major abnormalities in circulating lipoproteins and renal lipid metabolism. This article elaborates on the mechanisms of CKD and lipid uptake abnormalities. The viewpoint we supported is that lipid abnormalities directly cause CKD, resulting in forming a vicious cycle. On the theoretical and experiment fronts, this inference has been verified by elaborately elucidating the role of lipid intake and accumulation as well as their influences on CKD. Taken together, these findings suggest that further understanding of lipid metabolism in CKD may lead to novel therapeutic approaches.
Highlights
Lipids contain many molecules that contribute to structural components of membranes and signal transduction that regulates a variety of cellular events to maintain physiological homeostasis
Several studies have documented that chronic kidney disease (CKD) leads to decreased fatty acid oxidation (FAO), which could be an additional mechanism resulting in lipid accumulation [4]
After evaluating the population-based dietary pattern with the risk of incident CKD in a 6.1-year follow-up, it turned out that a high-fat, high-sugar diet was associated with an observable increase in the occurrence (46%) of incident CKD, whereas a lactovegetarian diet might be protective against the incidence of CKD by 43% [12]
Summary
Lipids contain many molecules that contribute to structural components of membranes and signal transduction that regulates a variety of cellular events to maintain physiological homeostasis. The increase in serum triglyceride to highdensity lipoprotein (HDL) ratio is a characteristic of dyslipidemia in CKD patients and is an independent indicator of disease progression. Several clinical studies have confirmed that an elevated serum triglyceride to HDL ratio has a major impact on the decrease of the estimated glomerular filtration rate (eGFR) and the development of CKD [2]. An increased abundance of saturated C16 or C20 free fatty acids (FFAs) accompanied by impaired β-oxidation has been noted in the late stage of CKD, contributing to further accumulation of saturated fatty acids (SFA) and leading to cell dysfunction, cell death, and the further progression of CKD [5]. Most studies emphasize the impact of lipid metabolism disorders in chronic kidney disease (CKD). This article focuses on the mechanism of lipid intake leading to CKD and possible therapeutic approaches
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