1. ¹INSERM U866, Faculté de Médecine, Dijon, France
2. ²IFR 100, Faculté de Médecine, Dijon, France
3. ³Centre d'hémodialyse, Hôpital du Bocage, Dijon, France
4. ⁴Department of Nephrology, Dialysis, and Renal Transplantation, CHU Saint Jacques, Besançon, France

Correspondence: D Masson or L Lagrost, INSERM U866, Faculté de Médecine, 7 Bd Jeanne d'arc, BP87900, Dijon 21079, France. E-mails: david.masson@chu-dijon.fr or Laurent.lagrost@u-bourgogne.fr

Received 28 September 2006; Revised 20 April 2007; Accepted 22 May 2007; Published online 1 August 2007.

Abstract

Apolipoprotein Cs (apoC-1, apoC-II, and apoC-III) are lipoprotein components that have regulatory effects on enzymes involved in lipoprotein metabolism. Owing to their low molecular weights, apoCs can adsorb onto and/or pass through dialysis membranes. Our study determines the consequence of hemodialysis (HD) on plasma concentrations of apoCs and on the activities of enzymes modulated by apoCs. Plasma samples were collected from 28 patients with chronic renal failure before and after HD. Plasma apoC-II levels were unchanged, whereas apoC-III levels were slightly decreased in post-dialysis plasmas. The apoC-I content was markedly reduced during HD. This was due to a significant decrease in the apoC-I content of very low-density lipoprotein (VLDL), whereas the apoC-I content of high-density lipoprotein (HDL) was unchanged. Although HDL bound apoC-I is thought to inhibit cholesterol ester transfer protein, no change in the ability of pre- and post-dialysis VLDL to interact with the transfer protein were observed. Complementary experiments confirmed that VLDL-bound apoC-I has no transfer protein inhibitory potential. In contrast, an increase in the ability of post-dialysis apoC-I-poor VLDL to act as substrate for lipoprotein lipase (LPL) was found compared to pre-dialysis VLDL. Our study shows that apoC-I losses during HD might be beneficial by improving the ability of VLDL to be a substrate for LPL thus improving plasma triglyceride metabolism.