Abstract 16528: Impact of Alirocumab on Apolipoprotein B, Non-High-Density Lipoprotein Cholesterol, and Triglycerides in Patients With and Without Moderate Chronic Kidney Disease
Introduction: Mixed dyslipidemia, characterized by high triglycerides (TGs) and non-high-density lipoprotein cholesterol (non-HDL-C), is frequently observed in chronic kidney disease (CKD) patients (pts). Given their high CV risk, CKD pts who cannot reach lipid goals with maximally tolerated statin doses may benefit from additional lipid-lowering therapy (LLT).
Objective: Assess impact of PCSK9 inhibitor alirocumab (ALI) on apolipoprotein B (apoB), non-HDL-C, and TGs in hypercholesterolemic pts with moderate CKD vs without (w/o).
Methods: Data analyzed from 8 ALI Phase 3 trials. All pts received stable background statin ± other LLT. Two trials (n=2448) compared ALI 150 mg Q2W vs placebo (PBO). Six trials (n=2181) compared ALI 75 mg Q2W vs PBO/ezetimibe; ALI was increased to 150 mg Q2W at W12 if LDL-C was ≥70 or ≥100 mg/dL at W8 depending on CV risk. Pts defined as having normal renal function/mild CKD (eGFR ≥90 or 60-89 mL/min/1.73 m2, respectively) were compared to those with moderate CKD (eGFR 30-59 mL/min/1.73 m2).
Results: Moderate CKD was present at baseline in 467/4629 (10.1%) pts. Reductions in apoB (% change from baseline at W24, LS means; range: CKD, -38.9:-54.8, w/out CKD, -38.2:-51.9), non-HDL-C (range: CKD, -39.2:-52.8, w/out, -40.7:-50.9), and fasting TGs (range: CKD, -12.1:-16.6, w/out, -8.5:-15.1) at W24 were observed in pts who received ALI (Figure). A larger reduction of apoB for ALI 150 mg vs PBO was observed in pts with moderate CKD vs w/out (interaction P-value 0.0033; Figure). Treatment-emergent adverse events (TEAEs) occurred in 82.1% ALI vs 82.8% control pts with moderate CKD (and 78.4 vs 78.2% w/o), SAEs in 23.0 vs 25.8% w/CKD (16.6 vs 16.2% w/o), and TEAEs led to discontinuation in 10.5 vs 7.3% w/CKD (6.2 vs 5.9% w/o).
Conclusion: In addition to similar LDL-C lowering with and w/out CKD as previously reported, ALI also reduced apoB, non-HDL-C, and TGs vs control, regardless of CKD status. The safety profile was similar in pts with and w/out moderate CKD.
Author Disclosures: P.P. Toth: Speakers Bureau; Modest; Kowa, Novartis, Sanofi-Aventis. Consultant/Advisory Board; Modest; Merck, Regeneron, Sanofi-Aventis. Speakers Bureau; Significant; Amarin, Amgen, Merck, Regeneron. Consultant/Advisory Board; Significant; Amgen, Kowa, Regeneron, Merck. M. Banach: Research Grant; Modest; Valeant. Speakers Bureau; Modest; Abbott, Mylan, Abbott Vascular, Actavis, Akcea, Amgen, KRKA, MSD, Sanofi-Aventis. Consultant/Advisory Board; Modest; Abbott Vascular, Amgen, Daiichi Sankyo, Esperion, MSD, Resverlogix, Sanofi-Aventis. A. Koren: Employment; Significant; Sanofi. M.J. Louie: Employment; Significant; Regeneron Pharmaceuticals, Inc. A. Letierce: Employment; Significant; Sanofi. J. Mandel: Other; Significant; Contractor for Sanofi mandated by IviData Stats. J.J. Kastelein: Consultant/Advisory Board; Modest; Sanofi, Amgen, Pfizer, Eli Lilly, The Medicines Company, Regeneron.
- © 2016 by American Heart Association, Inc.