title: Fluvastatin for dyslipoproteinemia, with or without concomitant chronic renal insufficiency.
abstract: Renal insufficiency is frequently associated with both quantitative and qualitative abnormalities in lipid and hemorheologic profiles. Although this may lead to increased risk of cardiovascular disease, a number of studies have also shown dyslipidemia to be a significant risk factor for the progression of renal insufficiency in human chronic renal disease. This double-blind, placebo-controlled trial aimed to assess the effect of fluvastatin, a synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on these parameters in dyslipidemic patients with or without chronic renal insufficiency. After a 6-week placebo run-in, 42 patients who had been previously stratified into 2 groups on the basis of creatinine clearance levels (0.5-1.0 mL/sec or > 1.0-1.5 mL/sec) were randomized to treatment with fluvastatin (40 mg daily) or matching placebo. Significant differences (on analysis of variance with repeated measures) were seen between fluvastatin and placebo treatment groups for changes in total cholesterol (-15% vs 1%, respectively; p < 0.001), low density lipoprotein cholesterol (LDL-C; -21% vs -5%; p < 0.001), very low density lipoprotein cholesterol (-14% vs 14%; p = 0.017), very low density lipoprotein triglycerides (-1% vs 29%; p = 0.014) and total triglycerides (-7% vs 24%; p < 0.001). These effects on cholesterol levels were reflected in a significant decrease in apolipoprotein B levels with fluvastatin therapy (p < 0.001). Apolipoprotein A-I levels increased (p = 0.054) despite no significant change in the levels of high density lipoprotein cholesterol. Response to therapy did not differ between the 2 renal function groups for any of the lipid, lipoprotein, and apolipoprotein variables. Hemorheologic parameters were not altered with fluvastatin therapy, regardless of renal function.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Lipid and Diabetes Research Group, Christchurch Hospital, New Zealand.
authors.forename: C J
authors.initials: CJ
authors.lastname: Lintott
authors.forename: R S
authors.initials: RS
authors.lastname: Scott
authors.forename: J M
authors.initials: JM
authors.lastname: Bremer
authors.forename: B I
authors.initials: BI
authors.lastname: Shand
mesh_terms: D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D016632:Apolipoprotein A-I / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D002784:Cholesterol / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood; D003404:Creatinine / Q000652:urine; D004311:Double-Blind Method; D005229:Fatty Acids, Monounsaturated / Q000627:therapeutic use*; D005260:Female; D000077340:Fluvastatin; D018056:Hemorheology; D006801:Humans; D006903:Hydroxymethylglutaryl CoA Reductases / Q000627:therapeutic use*; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D006951:Hyperlipoproteinemias / Q000097:blood / Q000150:complications* / Q000188:drug therapy*; D007211:Indoles / Q000627:therapeutic use*; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000503:physiopathology / Q000652:urine; D008079:Lipoproteins, VLDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D010919:Placebos; D012449:Safety; D014280:Triglycerides / Q000097:blood
chemical_list: D000924:Anticholesteremic Agents; D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D008078:Cholesterol, LDL; D015243:Cholesterol, VLDL; D005229:Fatty Acids, Monounsaturated; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D008079:Lipoproteins, VLDL; D010919:Placebos; D014280:Triglycerides; D000077340:Fluvastatin; D002784:Cholesterol; D003404:Creatinine; D006903:Hydroxymethylglutaryl CoA Reductases