title: Effects of atorvastatin on triglyceride-rich lipoproteins, low-density lipoprotein subclass, and C-reactive protein in hemodialysis patients.
abstract: Dyslipidemia is an important risk factor for cardiovascular disease in patients with chronic renal failure (CRF). We evaluated the safety and efficacy of atorvastatin in patients with dyslipidemia associated with CRF who were undergoing hemodialysis (HD). Thirty-five patients who were receiving HD were given atorvastatin (10 mg/d) for 3 months. Chylomicron (CM), light and dense very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and light and dense low-density lipoprotein (LDL) were separated by ultracentrifugation. Apolipoprotein (apo) B was measured by electroimmunoassay. Mean LDL particle diameter was measured by gradient gel electrophoresis. Atorvastatin therapy reduced LDL-cholesterol (C) by 36% and remnant-like particle (RLP)-C by 58%. Atorvastatin significantly reduced apo B, apo CIII, and apo E in VLDL by 40% to 46% and IDL-apo B by 66%. Atorvastatin also significantly reduced cholesterol in CM, light VLDL, and dense VLDL without consistently affecting triglyceride (TG) in these lipoproteins. Atorvastatin similarly reduced both light and dense LDL-apo B by 38%. LDL particle size in the HD patients significantly increased during atorvastatin treatment from 25.7 +/- 0.4 to 26.2 +/- 0.6 nm. High sensitive C-reactive protein (HS-CRP) was halved by atorvastatin decreasing from 0.08 +/- 0.05 to 0.04 +/- 0.03 mg/dL. Atorvastatin treatment did not affect the creatinine kinase level, and no classical adverse effects were observed during the study. These results suggest that atorvastatin is safe and effective for the management of dyslipidemia in patients with CFR who are receiving HD, which may help to suppress the development of atherosclerosis.
authors.affiliation: First Department of Internal Medicine, Showa University School of Medicine, Tokkyo, Japan.
authors.forename: Ayako
authors.initials: A
authors.lastname: Ikejiri
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Hirano
authors.forename: Satoru
authors.initials: S
authors.lastname: Murayama
authors.forename: Gen
authors.initials: G
authors.lastname: Yoshino
authors.forename: Natsuko
authors.initials: N
authors.lastname: Gushiken
authors.forename: Toru
authors.initials: T
authors.lastname: Hyodo
authors.forename: Takayasu
authors.initials: T
authors.lastname: Taira
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Adachi
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007676:Kidney Failure, Chronic / Q000097:blood / Q000628:therapy; D008074:Lipoproteins / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood*; D008079:Lipoproteins, VLDL / Q000097:blood; D010316:Particle Size; D011758:Pyrroles / Q000627:therapeutic use*; D006435:Renal Dialysis; D014280:Triglycerides / Q000097:blood*; D014657:Vasculitis / Q000188:drug therapy / Q000473:pathology
chemical_list: D001055:Apolipoproteins B; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008074:Lipoproteins; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; D011758:Pyrroles; D014280:Triglycerides; D002097:C-Reactive Protein; D002784:Cholesterol; D000069059:Atorvastatin; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D003402:Creatine Kinase