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NDT Advance Access published online on March 18, 2009

Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfp120
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© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org



Plasma phospholipid transfer protein, cholesteryl ester transfer protein and lecithin:cholesterol acyltransferase in end-stage renal disease (ESRD)

Madeleine V. Pahl, Zhenmin Ni, Lili Sepassi, Hamid Moradi and Nosratola D. Vaziri

Division of Nephrology and Hypertension, University of California, Irvine, CA, USA

Correspondence and offprint requests to: Madeleine V. Pahl; E-mail: mpahl{at}uci.edu



  Abstract

Background. Chronic kidney disease (CKD) results in accelerated atherosclerosis that is primarily caused by inflammation, oxidative stress and impaired triglyceride and HDL metabolisms. Several plasma proteins including phospholipid transfer protein (PTLP), cholesteryl ester transfer protein (CETP) and lecithin:cholesterol acyltransferase (LCAT) affect HDL metabolism. PLTP transfers phospholipids and free cholesterol from triglyceride-rich lipoproteins to HDL, phospholipids between HDL particles and facilitates cholesterol efflux from cells. CETP catalyzes the transfer of cholesteryl esters from HDL to LDL in exchange for triglycerides, and LCAT catalyzes esterification of free cholesterol on the surface of HDL. Given the role of these proteins in the regulation of HDL metabolism, we examined the effect of ESRD on plasma PLTL, CETP and LCAT.

Methods. A group of 21 stable ESRD patients maintained on haemodialysis and a group of 21 age-matched normal control individuals were included in the study. Plasma apolipoprotein A-1, PLTP, CETP and LCAT levels were measured.

Results. Plasma triglyceride concentration was elevated and plasma HDL cholesterol, apolipoprotein A-1 and LCAT concentrations were significantly reduced, whereas plasma PLTP and CETP concentrations and activities were unchanged in the ESRD patients.

Conclusions. These findings point to acquired LCAT and Apo A-1 deficiencies and tend to exclude dysregulation of PLTP or CETP in the pathogenesis of HDL abnormalities in haemodialysis patients.

Keywords: CETP; HDL metabolism; haemodialysis; LCAT; PL

Received for publication: 14.10.08
Accepted in revised form: 26. 2.09


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