Abstract
Although dyslipidemia is associated with chronic kidney disease (CKD), it is more common in nephrotic syndrome (NS), and guidelines for the management of hyperlipidemia in NS are largely opinion-based. In addition to the role of circulating lipids, an increasing number of studies suggest that intrarenal lipids contribute to the progression of glomerular diseases, indicating that proteinuric kidney diseases may be a form of “fatty kidney disease” and that reducing intracellular lipids could represent a new therapeutic approach to slow the progression of CKD. In this review, we summarize recent progress made in the utilization of lipid-modifying agents to lower renal parenchymal lipid accumulation and to prevent or reduce kidney injury. The agents mentioned in this review are categorized according to their specific targets, but they may also regulate other lipid-relevant pathways.
Highlights
Agents for the Treatment of Lipids are important constituents of cell membranes and play a pivotal role in energy production
Of the many lipid-relevant pathways of interest, we will focus our attention on cholesterol and fatty acid metabolism as we recently reviewed the role of sphingolipids in the progression of kidney diseases elsewhere [11]
We demonstrated that promoting ATP-binding cassette subfamily A member 1 (ABCA1)-mediated cholesterol efflux prevents renal disease progression in an experimental model of focal segmental glomerulosclerosis (FSGS) and of Alport syndrome (Col4a3 KO mice) in association with reduced formation of lipid droplets in glomeruli and reduced accumulation of cholesterol esters in kidney cortices
Summary
Agents for the Treatment of Lipids are important constituents of cell membranes and play a pivotal role in energy production. Patients with a gain-of-function mutation in the hydroxy-3-methylglutaryl-CoA reductase (HMGCR) gene, which codes for the rate-limiting enzyme of the cholesterol synthesis pathway, do not develop kidney disease [13]. Tangier disease is a rare autosomal recessive disorder associated with mutations in the ATP-binding cassette subfamily A member 1 (ABCA1) [16], and patients with the disease present with a decrease in high-density lipoproteins (HDL), accumulation of cholesterol esters in multiple organs, mild proteinuria and foamy podocytes in kidney biopsies [17]. Missense mutation of the LIM homeobox transcription factor 1 beta (LMX1β) causes nail-patella-like renal disease This mutation is associated with reduced ABCA1 and ABCG1 expression and increased lipid droplet accumulation in podocytes, leading to podocyte injury [18]. If and how APOL1 risk variants are associated with kidney diseases through altered lipid metabolism remains to be established
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