Abstract
Since the lipid nephrotoxicity hypothesis was proposed in 1982, increasing evidence has supported the hypothesis that lipid abnormalities contributed to the progression of both atherosclerosis and glomerulosclerosis. In this chapter, we discussed the promises of and exceptions to the original hypothesis and update the hypothesis by describing how inflammatory stress accompanying CKD fundamentally modifies cholesterol homeostasis, causing lipid redistribution and renal vascular injury, and also causes statin resistance. This concept alters traditional understanding of the pathogenesis of lipid-mediated renal and vascular injury, and evaluation of renal and cardiovascular risk and lipid-lowering treatment in such patients.
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