title: Severe defect in clearing postprandial chylomicron remnants in dialysis patients.
abstract: Lipid abnormalities have been suggested as a major cause of the accelerated atherosclerosis and the high incidence of coronary heart disease in chronic renal failure patients. In the present work the postprandial lipoprotein metabolism was studied in chronic dialysis patients with or without fasting hypertriglyceridemia using the vitamin A loading test. This method investigates specifically postprandial lipoprotein metabolism. The determination of vitamin A ester level retinyl palmitate (RP) differentiates the circulating plasma chylomicron and chylomicron remnant fractions from the endogenous VLDL and IDL. Subjects with normal renal function with or without fasting hypertriglyceridemia served as control groups. Dialysis patients have significantly higher level of chylomicron remnants for a more prolonged period of time than controls, irrespective of their fasting triglyceride levels. The area below retinyl palmitate chylomicron remnants curve was 26308 +/- 12422 micrograms/liter.hr in the normolipidemic dialysis patients, significantly higher than (6393 +/- 2098 micrograms/liter.hr; P < 0.0001) in the normolipidemic controls. The retinyl palmitate chylomicron remnants curve of the hypertriglyceridemic dialysis patients was 21021 +/- 4560 micrograms/liter.hr, which was higher than 12969 +/- 2215 micrograms/liter.hr (P < 0.0001) in the hypertriglyceridemic controls. Moreover, the hypertriglyceridemic dialysis patients had an additional defect in the lipolysis metabolic step, that is, accumulation of chylomicrons in circulation. These findings show a severe defect in postprandial lipoprotein metabolism in chronic renal failure patients. The prolonged exposure of the vascular wall to high chylomicron remnant concentrations might be an important pathogenetic factor in the accelerated atherosclerosis seen in chronic dialysis patients.
authors.affiliation: Department of Nephrology, Tel Aviv Medical Center, Israel.
authors.forename: M
authors.initials: M
authors.lastname: Weintraub
authors.forename: A
authors.initials: A
authors.lastname: Burstein
authors.forename: T
authors.initials: T
authors.lastname: Rassin
authors.forename: M
authors.initials: M
authors.lastname: Liron
authors.forename: Y
authors.initials: Y
authors.lastname: Ringel
authors.forename: S
authors.initials: S
authors.lastname: Cabili
authors.forename: M
authors.initials: M
authors.lastname: Blum
authors.forename: G
authors.initials: G
authors.lastname: Peer
authors.forename: A
authors.initials: A
authors.lastname: Iaina
mesh_terms: D000328:Adult; D001161:Arteriosclerosis / Q000209:etiology; D002914:Chylomicrons / Q000097:blood / Q000378:metabolism*; D003327:Coronary Disease / Q000209:etiology; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism* / Q000628:therapy; D008074:Lipoproteins / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D010531:Peritoneal Dialysis, Continuous Ambulatory / Q000009:adverse effects; D006435:Renal Dialysis / Q000009:adverse effects*; D014280:Triglycerides / Q000097:blood
chemical_list: D002914:Chylomicrons; D008074:Lipoproteins; D014280:Triglycerides