Dyslipidemia in chronic kidney disease: Causes and consequences G.A. Kaysen  Kidney International  Volume 70, Pages S55-S58 (December 2006) DOI: 10.1038/sj.ki.5001979 Copyright © 2006 International Society of Nephrology Terms and Conditions

Figure 1 Lipoprotein metabolism: HDL is assembled through the combination of cholesterol, phospholipids, and apo A I, produced in the liver and gut. Cholesterol is incorporated in part by the action of the adenosine triphosphate-binding cassette-1 and is then esterified by lecithin CE transfer protein (LCAT) allowing HDL to enlarge into spherical HDL3 and HDL2. VLDL is secreted by the liver and processed on the vascular endothelium by LPL. LPL is activated by apo C II and inhibited by apo C III. CMs are secreted by the gut. Phospholipids released by lipolysis of both CM and VLDL contribute to the formation of small dense pre β or discoidal HDL and the VLDL remnant particle is either taken up directly by the liver through the lipoprotein-like receptor or is transformed into LDL by action of CE transfer protein, exchanging the CE-rich core of HDL with VLDL TGs. CM remnants are taken up by the liver. TG-rich HDL is then processed by HL into smaller dense HDL. Mature HDL2 either transfers CEs to the liver by interaction with the scavenger receptor B-1 or transfers its CE-rich core to VLDL remnants creating LDL. Small dense pre β or discoidal HDL is subject to accelerated degradation in part by the kidney. Kidney International 2006 70, S55-S58DOI: (10.1038/sj.ki.5001979) Copyright © 2006 International Society of Nephrology Terms and Conditions