Acute kidney injury in statin initiators
- PMID: 23960024
- PMCID: PMC3822439
- DOI: 10.1002/pds.3500
Acute kidney injury in statin initiators
Abstract
Purpose: Statins are widely used for preventing cardiovascular disease, yet recent reports suggest an increased risk of acute kidney injury (AKI). We estimated the one-year risk of AKI associated with statin initiation and determined the comparative safety of individual statin formulations.
Methods: We performed a cohort study in insurance billing data from commercial and Medicare insurance plans in the United States for the years 2000-2010. We identified statin initiators and non-users with histories of medication use and healthcare utilization. AKI diagnosis codes were identified in the one year following the index date. We estimated hazard ratios (HR) and 95% confidence intervals (CI) with adjusted and propensity score (PS)-matched Cox-proportional hazards models. Models were run separately in insurance groups and adjusted for cardiovascular and renal risk factors, markers of healthcare utilization, and other medication use.
Results: We identified 3,905,155 statin initiators and 2,817,621 eligible non-users. The adjusted HR of AKI in statin initiators compared to non-users was: commercial, HR = 1.04 (95% CI: 0.99, 1.09); Medicare, HR = 0.72 (95% CI: 0.70, 0.75). PS-matching yielded: commercial, HR = 0.82 (95% CI: 0.78, 0.87); Medicare, HR = 0.66 (95% CI: 0.63, 0.69). As individual formulations, higher-potency simvastatin was associated with an increased risk of AKI over lower-potency simvastatin in adjusted models: commercial, HR = 1.42 (95% CI: 1.28, 1.58); Medicare, HR = 1.24 (95% CI: 1.15, 1.35).
Conclusions: As a class, statin initiation was not associated with an increase in AKI. However, higher-potency simvastatin did exhibit an increased AKI risk.
Keywords: acute kidney injury; comparative effectiveness; drug safety; pharmacoepidemiology; propensity scores.
Copyright © 2013 John Wiley & Sons, Ltd.
Conflict of interest statement
Dr. Brookhart has served on scientific advisory boards for Pfizer, with honoraria either donated to charity or received by UNC.
Dr. Simpson has received research support from Merck, and honoraria for lectures from Merck and Pfizer.
Dr. Jonsson Funk: GlaxoSmithKline (GSK) has a collaborative agreement with the Center for Pharmacoepidemiology, Department of Epidemiology, UNC Chapel Hill. GSK does not review any research nor provide any input into the analysis of the drug classes being studied.
Dr. Stürmer receives investigator-initiated research funding and support as Principal Investigator (RO1 AG023178) and Co-Investigator (RO1 AG018833) from the National Institute on Aging at the National Institutes of Health. He also receives research funding as Principal Investigator of the UNC-DEcIDE center from the Agency for Healthcare Research and Quality. Dr. Stürmer does not accept personal compensation of any kind from any pharmaceutical company, though he receives salary support from the Center for Pharmacoepidemiology in the Department of Epidemiology at UNC and from unrestricted research grants from pharmaceutical companies to UNC.
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