title: Reduction of intermediate density lipoprotein by pravastatin in hemo- and peritoneal dialysis patients.
abstract: Elevated plasma intermediate density lipoprotein (IDL) is one of the features of uremic dyslipidemia which is potentially atherogenic. We examined the effects of pravastatin, an HMG-CoA reductase inhibitor, on IDL levels as well as other lipoprotein parameters in 19 uremic patients treated with hemodialysis (HD, n = 11) or continuous ambulatory peritoneal dialysis (CAPD, n = 8). The patients were administered 5 mg/day pravastatin for the initial 4 weeks and 10 mg/day for the subsequent 12 weeks. In the analysis of the total subjects, IDL-cholesterol was reduced by 31% as well as low density lipoprotein (LDL)-cholesterol. Cholesterol in very low density lipoprotein (VLDL) also decreased whereas that in high density lipoprotein (HDL) did not. Significant decrease of serum triglycerides was due mainly to reduced IDL- and LDL-triglycerides. Apolipoprotein (apo) A-I did not change, whereas apo A-II, B, C-II, C-III, E, and B/A-I ratio were significantly lowered. Pravastatin did not affect measured activity of lecithin: cholesterol acyltransferase, post-heparin plasma lipoprotein lipase or hepatic triglyceride lipase. HD and CAPD patients responded almost equally to the treatment. IDL elevation was present independent of serum total cholesterol, and it was lowered by pravastatin even in non-hypercholesterolemic subjects. There was no critical adverse effect besides transient and asymptomatic increase of serum creatine kinase level. We conclude that pravastatin can be a safe and effective approach to the management of dyslipidemia in uremic patients who have an elevated level of IDL.
authors.affiliation: Second Department of Internal Medicine, Osaka City University Medical School, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Nishizawa
authors.forename: T
authors.initials: T
authors.lastname: Shoji
authors.forename: M
authors.initials: M
authors.lastname: Emoto
authors.forename: K
authors.initials: K
authors.lastname: Kawasaki
authors.forename: T
authors.initials: T
authors.lastname: Konishi
authors.forename: T
authors.initials: T
authors.lastname: Tabata
authors.forename: T
authors.initials: T
authors.lastname: Inoue
authors.forename: H
authors.initials: H
authors.lastname: Morii
mesh_terms: D001053:Apolipoproteins / Q000097:blood; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood; D005260:Female; D006801:Humans; D008049:Lipase / Q000378:metabolism; D008071:Lipoprotein Lipase / Q000097:blood; D008074:Lipoproteins / Q000097:blood*; D053419:Lipoproteins, IDL; D008099:Liver / Q000201:enzymology; D008297:Male; D008875:Middle Aged; D010531:Peritoneal Dialysis, Continuous Ambulatory; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000097:blood; D017035:Pravastatin / Q000008:administration & dosage / Q000494:pharmacology*; D006435:Renal Dialysis; D014280:Triglycerides / Q000097:blood; D014511:Uremia / Q000097:blood / Q000628:therapy
chemical_list: D001053:Apolipoproteins; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D015243:Cholesterol, VLDL; D008074:Lipoproteins; D053419:Lipoproteins, IDL; D014280:Triglycerides; C030104:lipoprotein cholesterol; D002784:Cholesterol; D007862:Phosphatidylcholine-Sterol O-Acyltransferase; D008049:Lipase; D008071:Lipoprotein Lipase; D017035:Pravastatin