Author + information
- Michael Böhm, MD∗ (, )
- Michael D. Ezekowitz, MB ChB, DPhil,
- Stuart J. Connolly, MD,
- John W. Eikelboom, MBBS,
- Stefan H. Hohnloser, MD,
- Paul A. Reilly, PhD,
- Helmut Schumacher, PhD,
- Martina Brueckmann, MD,
- Stephan H. Schirmer, MD, PhD,
- Mario T. Kratz, MD,
- Salim Yusuf, MD, DPhil,
- Hans-Christoph Diener, MD,
- Ziad Hijazi, MD and
- Lars Wallentin, MD, PhD
- ↵∗Uniklinikum des Saarlandes, Cardiology, Kirrbergerstrasse, Homburg, Saarland 66421, Germany
We thank Dr. Yang and colleagues for their interest in our analysis of changes in renal function in the RE-LY (Randomized Evaluation of Long Term Anticoagulant Therapy) study over time in patients with atrial fibrillation treated with dabigatran or warfarin (1).
We agree that kidney function must be monitored closely in patients receiving oral anticoagulants. The differential effects of dabigatran and warfarin that Dr. Yang and colleagues reference are from animal models that, although interesting, may not represent patients. The rat study comparing those having five-sixth of their kidney removed with controls, with both receiving high doses of dabigatran, led to an increase in serum creatinine and hematuria (2). This is expected with supratherapeutic dabigatran doses and severe renal failure. In humans, severe renal function is a contraindication for dabigatran. To date, there is no evidence of dabigatran-induced renal injury in animals or humans. In our subanalysis from the RE-LY study (1), the decline in renal function corresponds well to the physiological decline seen in elderly populations. We believe, therefore, that there is no evidence to support renal toxicity in patients prescribed dabigatran in approved doses in patients with a creatinine clearance >15 ml/min. We do believe that monitoring renal function is critical to avoid prescribing dabigatran at inappropriate doses or at all if renal function does decline, which can occur for multiple well-known reasons independent of dabigatran administration.
Please note: RE-LY was funded by Boehringer Ingelheim, Germany. All authors received scientific support from Boehringer Ingelheim. Dr. Böhm is supported by the Deutsche Forschungsgesellschaft (KFO 196). Drs. Schumacher and Brueckmann are employees of Boehringer Ingelheim, Germany. Dr. Reilly is an employee of Boehringer Ingelheim, USA.
- 2015 American College of Cardiology Foundation