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J Am Coll Cardiol. 2015 Jun 16;65(23):2481-93. doi: 10.1016/j.jacc.2015.03.577.

Changes in Renal Function in Patients With Atrial Fibrillation: An Analysis From the RE-LY Trial.

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Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Homburg, Germany. Electronic address:
Sidney Kimmel Medical College at Jefferson University, Philadelphia, Pennsylvania; Lankenau Institute for Medical Research and The Heart Center, Wynnewood, Pennsylvania.
Population Health Research Institute, McMaster University and Hamilton Health Sciences, Hamilton, Ontario, Canada.
Department of Cardiology, J.W. Goethe University, Frankfurt/Main, Germany.
Boehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut.
Boehringer Ingelheim Pharma GmbH & Co. KG, Ingelheim, Germany.
Boehringer Ingelheim Pharma GmbH & Co. KG, Ingelheim, Germany; Faculty of Medicine Mannheim at the University of Heidelberg, Heidelberg, Germany.
Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Homburg, Germany.
Department of Neurology, Universitätsklinikum Duisburg-Essen, Essen, Germany.
Uppsala Clinical Research Center and Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden.



Vitamin K-dependent factors protect against vascular and renovascular calcification, and vitamin K antagonists may be associated with a decreased glomerular filtration rate (GFR).


This study analyzed changes in GFR during long-term treatment with warfarin or dabigatran etexilate (DE) in patients enrolled in the RE-LY (Randomized Evaluation of Long Term Anticoagulation Therapy) trial.


Of the 18,113 patients in the RE-LY study randomized to receive DE (110 mg or 150 mg twice daily) or warfarin, 16,490 patients with atrial fibrillation had creatinine values measured at baseline and at least 1 follow-up visit. Changes in GFR for up to 30 months were evaluated.


GFR declined in all treatment groups. After an average of 30 months, the mean ± SE decline in GFR was significantly greater with warfarin (-3.68 ± 0.24 ml/min) compared with DE 110 mg (-2.57 ± 0.24 ml/min; p = 0.0009 vs. warfarin) and DE 150 mg (-2.46 ± 0.23 ml/min; p = 0.0002 vs. warfarin). A decrease in GFR >25% was less likely with DE 110 mg (hazard ratio: 0.81 [95% confidence interval: 0.69 to 0.96]; p = 0.017) or DE 150 mg (hazard ratio: 0.79 [95% confidence interval: 0.68 to 0.93]; p = 0.0056) than with warfarin in the observation period >18 months. Patients with poor international normalized ratio control (i.e., time in therapeutic range <65%) exhibited a faster decline in GFR. A more pronounced decline in GFR was associated with previous warfarin use and with the presence of diabetes.


Patients with atrial fibrillation receiving oral anticoagulation exhibited a decline in renal function that was greater in those taking warfarin versus DE, and it was amplified by diabetes and previous vitamin K antagonist use. (Randomized Evaluation of Long Term Anticoagulant Therapy [RE-LY] With Dabigatran Etexilate; NCT00262600).


anticoagulation; atrial fibrillation; renal function; thrombin inhibition; vitamin K antagonist

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