A defect in cholesterol transport was detected in patients with uremia who were receiving long-term hemodialysis when the rate of cholesterol transfer (RCT) from high-density lipoprotein (HDL) to very low-density (VLDL) and low-density lipoproteins (LDL) was compared with that in controls. The RCT (mean ± SD) in 29 men with uremia (1.85 ± 1.29 mg/hr/100 ml) and 11 women with uremia (1.84 ± 1.00 mg/hr/100 ml) was significantly lower (P < 0.001) than values in 55 healthy men (4.50 ± 2.61 mg/hr/100 ml) and 23 healthy women (3.72 ± 1.92 mg/hr/100 ml), respectively. Six patients, but none of the controls, totally lacked the ability for cholesterol transfer. The decreased RCT of the patients could not be completely accounted for by their decreased HDL cholesterol levels, because patients matched with controls for HDL cholesterol within 1 mg/100 ml also had lower RCT (P < 0.0025). Recombination and crossover of serum fractions of patients and controls separated by ultracentrifugation revealed that the defect in cholesterol transfer of the patients was in the d > 1.063 gm/ml fraction (containing HDL and other serum proteins), which not only contained less HDL cholesterol, but was also qualitatively inferior as donor for cholesterol transfer. In one of four patients studied, the d < 1.063 gm/ml fraction (VLDL and LDL) also had deficient ability to accept cholesteryl esters in the transfer. These in vitro data indicate a defect in cholesterol transport in the patients who are undergoing hemodialysis. Whether this defect exists in vivo creates the risk of accelerated atherosclerosis warrants further study.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of Laboratory and Clinical Medicine|
|State||Published - Dec 1 1985|
ASJC Scopus subject areas
- Pathology and Forensic Medicine