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Updated: Aug 19, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
[Studies on the factors responsible for low erythrocyte alpha-tocopherol concentrations in patients on maintenance
Abstract:
The present study was undertaken to clarify the low erythrocyte (RBC) alpha-tocopherol (TOC) concentrations in patients on maintenance hemodialysis (HD) using in vivo and in vitro experiments. 15 age-matched male controls and HD patients were evaluated. The experimental designs and the results were as follows: 1) Changes in fasting stage; TOC levels of plasma, high density lipoproteins (HDL) and RBC, especially RBC, were lower in HD-patients than in controls. The ratio of RBC to plasma and HDL showed more significant changes between HD-patients and controls. In controls, RBC-TOC was noted to have a positive correlation with HDL-TOC and a negative correlation with non HDL-(plasma--HDL)-TOC, whereas a reverse correlation was observed in HD-patients. 2) In vivo experiments: Each 7 of HD-patients and controls were orally given TOC 600 mg after meal at early morning; the blood was sampled at 0, 3, 6, 10 and 24 hr. Poor increase of RBC-TOC in HD-patients was observed. In contrast, HDL-TOC was significantly higher at all measurement times than in controls. The change of plasma-TOC was similar to that of non HDL-TOC. 3) In vitro experiment:RBC from patients or controls showing various concentrations of RBC-TOC and plasma from controls were incubated at 37 degrees C or 4 degrees C. The inactivated plasma from controls was prepared by incubation at 56 degrees C, 30 min or by supplement of 2 mM parachloromerucuric benzonic sulfonate. The ratio of RBC and plasma was at 2:3 close to physiological conditions. No difference between patient and control RBCs as an acceptor of TOC and no appreciable transfer of TOC between RBC to plasma at 4 degrees C were observed. When RBC-TOC was low, transfer volume of TOC from plasma to RBC was increased and TOC was supplied from mainly non HDL fractions; in contrast, when it was high, the main source of TOC was due to the transfer from HDL fractions which was reduced when lecithin: cholesterol acyltransferase (LCAT) reaction was inhibited. From above in vivo and in vitro studies, it was concluded that low levels of RBC-TOC in HD-patients may be due to an insufficiency of TOC transfer from HDL fractions affected by low LCAT activity.
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