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.

Chronic kidney disease delays VLDL-apoB-100 particle catabolism: potential role of apolipoprotein C-III

“…We observed clearance defects in total VLDL, VLDL 1 , and VLDL 2 apoB-100 without changes in production rates, suggesting that VLDL (total and subclass) apoB-100 overproduction in CKD subjects is possibly this relationship may partly relate to abnormal metabolism of apoC-III or a hitherto unidentifi ed uraemic toxin. The association between apoC-III and apoB-48 in the CKD subjects suggest that apoC-III may contribute to postprandial hypertriglyceridemia and accumulation of chylomicron remnants ( 43,44 ). This needs further investigation.…”

Impaired triglyceride tolerance in hemodialysis patients with different apolipoprotein E (apo E) isoforms.

“…These changes in lipid parameters indicated a delayed degradation of the administered fatty load 8 . The most significant changes were evident in the subgroup of apo E2/3 uremic pts, reflecting their higher fasting TG concentration.…”

Etiology and management of dyslipidemia in children with chronic kidney disease and end-stage renal disease

“…The impact of CKD/ESRD on postprandial lipoprotein metabolism is still under study. In studies of patients with CKD, there is a greater rise and an abnormally prolonged increase in circulating triglycerides postprandially [20,69].…”