Nephrology Dialysis Transplantation, Vol 12, Issue 1 87-92, Copyright © 1997 by Oxford University Press
R Walker, W Sutherland, H Walker, S MacMahon and R Robson
Background. Plasma cholesteryl ester transfer activity
is increased in patients with chronic renal failure on dialysis who have
elevated levels of apolipoprotein B (apoB)-containing lipoproteins.
Simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase
inhibitor, reduces levels of these lipoproteins but the effect of treatment
on cholesteryl ester transfer activity in patients on dialysis remains to
be determined. Methods. We measured serum newly
synthesized cholesteryl ester transfer (NCET) activity,
lecithin:cholesterol acyltransferase (LCAT) activity and serum lipid,
lipoprotein and apolipoprotein concentrations before and immediately after
6 months of treatment with simvastatin (10 mg daily, n=24) or placebo
(n=29) in 53 patients with chronic renal failure receiving haemodialysis or
continuous ambulatory peritoneal dialysis (CAPD).
Results. Simvastatin therapy significantly reduced
serum cholesterol, LDL cholesterol, apoB concentrations, and both NCET
(P=0.001) and LCAT (P=0.012) rates. The decrease in NCET activity was
correlated significantly with the corresponding decrease in apoB
concentration (r=0.715, P <0.001) during simvastatin therapy and was
no longer significant when apoB concentration (P=0.14) or LCAT activity
(P=0.07) were controlled. Conclusion. These data show
that simvastatin therapy reduces serum NCET rates, and suggest that this
may be linked to the concomitant decrease in levels of apoB-containing
lipoproteins which are acceptors of transferred cholesteryl esters, and to
the decrease in serum LCAT rates in patients with chronic renal failure
with treatment. Keywords: cholesteryl ester transfer;
dialysis; simvastatin
ORIGINAL ARTICLES
Effect of treatment with simvastatin on serum cholestryl ester transfer in patients on dialysis
Department of Medicine, University of Otago Medical School, Dunedin, New Zealand; Clinical Trials Research Unit, Department of Medicine, University of Auckland, New Zealand; Corresponding author at: Department of Medicine, University of Otago Medical School, PO Box 913, Dunedin, New Zealand
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