Effects of atorvastatin on Lp(a) and lipoprotein profiles in hemodialysis patients.
BACKGROUND
Dialysis patients have many underlying traditional and nontraditional risk factors that may predispose them to a high prevalence of cardiovascular disease. The effects of statins (eg, atorvastatin) on altering nontraditional lipoprotein measures in dialysis patients have not been extensively investigated.


OBJECTIVE
To evaluate the efficacy of atorvastatin compared with a control group in inducing changes in lipoprotein(a) [Lp(a)], apolipoprotein (Apo) A-1, Apo-B, and fibrinogen levels, as well as the conventional lipoprotein profile, in hemodialysis patients over 36 weeks; secondary objectives were to assess changes in C-reactive protein, albumin, and safety measures.


METHODS
Forty-five hemodialysis patients with low-density lipoprotein cholesterol (LDL-C) levels greater than 100 mg/dL were randomized to parallel groups: atorvastatin (n = 19) or no treatment (n = 26). The atorvastatin dose was titrated from 10 mg to achieve an LDL-C goal of 100 mg/dL or less and therapy was continued for 36 weeks. Biochemical and lipoprotein laboratory tests for efficacy outcomes were obtained at baseline, 12 weeks, and 36 weeks.


RESULTS
The atorvastatin group exhibited clinically significant reductions (mean +/- SD) compared with controls in total cholesterol (-21.7 +/- 41.7 vs -3.2 +/- 40.0 mg/dL, respectively; p = 0.017) and LDL-C (-13.1 +/- 32.0 vs -1.1 +/- 38.4 mg/dL, respectively; p = 0.058) levels, as well as Lp(a) (-10.6 +/- 27 vs 3.5 +/- 17.8 mg/dL, respectively; p = 0.046). Statistical analyses included analysis of variance on ranked measures for multivariable modeling and paired t-test to determine changes in efficacy measures between baseline and 36 weeks within groups.


CONCLUSIONS
Atorvastatin was safe and effective in reducing Lp(a), total cholesterol, and LDL-C levels. Given the prevalence of atherosclerosis in hemodialysis patients, therapy aimed at reducing traditional and nontraditional risk factors may be beneficial.
Joy
Melanie S
MS
Division of Nephrology and Hypertension, School of Medicine, University of North Carolina Kidney Center, University of North Carolina, Chapel Hill, NC 27599, USA. Melanie_Joy@med.unc.edu
Dornbrook-Lavender
Kimberly A
KA
Chin
Hyunsook
H
Hogan
Susan L
SL
Denu-Ciocca
Cynthia
C
D000368:Aged; D000924:Anticholesteremic Agents / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D016632:Apolipoprotein A-I / Q000187:drug effects; D001055:Apolipoproteins B / Q000187:drug effects; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000187:drug effects / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005260:Female; D005340:Fibrinogen / Q000187:drug effects; D006538:Heptanoic Acids / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D006801:Humans; D006937:Hypercholesterolemia / Q000188:drug therapy*; D017270:Lipoprotein(a) / Q000187:drug effects; D008074:Lipoproteins / Q000097:blood / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*; D006435:Renal Dialysis; D012709:Serum Albumin / Q000187:drug effects
D000924:Anticholesteremic Agents; D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D017270:Lipoprotein(a); D008074:Lipoproteins; D011758:Pyrroles; D012709:Serum Albumin; D005340:Fibrinogen; D002097:C-Reactive Protein; D002784:Cholesterol; D000069059:Atorvastatin