New insights into lipid metabolism in chronic kidney disease.

Disorders in lipid levels in kidney disease consist of alterations both in the levels of the differing lipoprotein classes as well as alteration in their structures. Triglycerides (TGs) are increased, and both high density lipoprotein (HDL) and low density lipoprotein (LDL) levels are reduced. HDL fails to mature normally primarily as a consequence of decreased activity of lecithin cholesterol ester transfer protein (LCAT), and HDL levels are reduced because of increase clearance. The HDL that is present consist of small pre-β discoid HDL that fails to function as an antioxidant. All of the apo B containing lipoproteins exhibit decreased clearance in part because of increased levels of the lipoprotein lipase inhibitory apolipoproteins apo C I and apo C III. The concentration of oxidized LD, an athorgenic risk factor, is increased, in part because of the inability of the HDL that is present to reduce oxidized LDL and in part because of the increased LDL residence time effected by decreased clearance.