Key result
Dyslipidemia and altered intracellular lipid handling in metabolic syndrome and chronic kidney disease contribute to glomerulosclerosis, interstitial fibrosis, and accelerated disease progression.
This review highlights the mechanisms by which dyslipidemia in metabolic syndrome and CKD contributes to renal disease progression and increased cardiovascular mortality.
Does not support immediate changes to lipid therapy in CKD; leaves open whether targeting dyslipidemia slows renal progression.
Metabolic syndrome is associated with dyslipidemia, which is thought to contribute in part to the development of chronic kidney disease (CKD). This review discusses the factors that regulate intracellular handling of lipids and their relationship to disordered mesangial cell function. Specific attention is paid to those factors such as fatty acid translocase/scavenger receptor BII, proliferator-activated receptor delta, insulin-like growth factor-1, inflammation and hypertriglyceridemia that are altered in the metabolic syndrome. CKD also causes an increase in triglycerides and a decrease in high-density lipoprotein that mimic the lipid abnormalities of metabolic syndrome, which accelerate the progression of CKD and increase the risk for cardiovascular mortality. There is a special emphasis on foam cells in the kidney and lipid-mediated changes in intrinsic kidney cells that lead to glomerulosclerosis and interstitial fibrosis. Correlates to whole animal and humans studies are included.
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Christine K. Abrass (2006) conducted a review in Chronic kidney disease and metabolic syndrome. Dyslipidemia was evaluated. Dyslipidemia and altered intracellular lipid handling in metabolic syndrome and chronic kidney disease contribute to glomerulosclerosis, interstitial fibrosis, and accelerated disease progression.
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