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Plasma lipoproteins and lecithin:cholesterol acyltransferase distribution in patients on dialysis
Insights
Patients on chronic hemodialysis exhibit decreased high-density lipoprotein (HDL) cholesterol and lower lecithin-cholesterol acyltransferase (LCAT) activity, potentially impairing lipid metabolism in uremia.
Area of Science:
- Nephrology
- Lipid Metabolism
- Biochemistry
Background:
- Chronic hemodialysis patients often present with dyslipidemia.
- Lecithin-cholesterol acyltransferase (LCAT) plays a crucial role in high-density lipoprotein (HDL) metabolism.
Purpose of the Study:
- To investigate plasma lipoprotein profiles and LCAT activity in patients undergoing chronic hemodialysis.
- To explore potential genetic factors influencing hypertriglyceridemia in this patient group.
Main Methods:
- Utilized spin density gradient separation and exogenous substrate enzyme assays.
- Analyzed apolipoprotein ratios (ApoE3/E2, ApoCII/CIII) to assess genetic influences.
- Conducted a 1-year follow-up study to confirm findings.
Main Results:
- Hemodialysis patients showed significantly reduced HDL cholesterol and plasma LCAT activity compared to controls.
- LCAT activity was primarily associated with HDL and VHDL fractions in both groups.
- No significant genetic differences in ApoE3 heterozygosity were found; ApoCII/CIII ratios showed a trend towards lower values in patients.
- Follow-up study confirmed decreased HDL and LCAT activity.
Conclusions:
- Reduced LCAT activity and low HDL cholesterol in hemodialysis patients may contribute to impaired lipolysis.
- LCAT activity measured with an exogenous substrate is decreased in uremic patients, but not when measured with an endogenous substrate.
Abstract:
Plasma lipoproteins and LCAT activity were studied using a single spin density gradient separation and an exogenous substrate enzyme assay in 41 patients on chronic hemodialysis and in 11 normal subjects. The plasma HDL cholesterol was markedly decreased (33 vs. 63 mg/dl, P less than 0.001) while total and LDL-cholesterol were unchanged in the patients. Plasma LCAT activity was significantly lower in the patient group (42 vs. 59 nmoles/4 hr/ml, P less than 0.001), but the distribution of activity (studied in 13 dialysis patients and 12 control subjects) was not different between the two groups: 90% being associated with HDL and VHDL lipoprotein fractions. To examine the possible genetic influence on the development of hypertriglyceridemia in the patient group, we examined the ratio of apolipoproteins E3/E2 and CII/CIII in ten of the patients and another group of 13 control subjects. The frequency of heterozygotes for E3 deficiency was not different between the patient (one of ten) and the control (two of 13) groups. While the patient group had lower CII/CIII ratio, the figures did not reach statistical significance. The low LCAT activity in the face of higher plasma triglycerides and low HDL may contribute to impaired lipolysis previously documented in uremic patients. A follow-up study performed 1 year after the initial study confirmed the decreased HDL (51 vs. 71 mg/dl, P less than 0.01) and LCAT activity (50 vs. 59 nmoles/hr/ml, P less than 0.02) in an exogenous substrate system (N = 20). LCAT measured using the endogenous substrate was not significantly different from the control group (49 vs. 55 nmoles/hr/ml).(ABSTRACT TRUNCATED AT 250 WORDS)