New data indicate that kidney function decline is less pronounced in patients with non-valvular atrial fibrillation who are treated with Pradaxa (dabigatran etexilate) compared to warfarin. A natural decline in kidney function is expected as part of the ageing process or as a result of other underlying diseases. New data support that long-term Pradaxa treatment compares favourably to warfarin in terms of kidney function decline over time. The new RE-LY study sub-analysis findings were presented at a Clinical Trial Update Hot Line session during the ESC Congress 2014 in Barcelona, Spain.
“These data support dabigatran as a good long-term treatment option for non-valvular atrial fibrillation patients,” says Professor Michael Böhm, director of the Department of Internal Medicine and Cardiology at the University Hospital of Saarland, Homburg/Saar, Germany. “These RE-LY study findings may have particular relevance for NVAF patients who have co-existing medical conditions which negatively impact their kidney function, such as diabetes, and for patients with poorly controlled vitamin K antagonist therapy. Dabigatran may provide additional benefit to these patients in the long term.”
The data included in the ESC Congress 2014 Hot Line session were derived from a post hoc exploratory analysis of the RE-LY study that included over 18,000 patients and compared kidney function change in patients treated with either warfarin or Pradaxa (110mg or 150mg twice daily).
Results indicate that kidney function deteriorated more in patients on warfarin compared to those on either dose of Pradaxa. Results were significantly different to warfarin for both doses of Pradaxa at 30 months, with similar patterns seen in different Pradaxa subgroups. Patients who were poorly controlled on warfarin and spent more time above the recommended International Normalized Ratio target range (INR 2-3) experienced a markedly sharper decline in kidney function compared to patients taking Pradaxa. Patients with diabetes, who are at generally higher risk of kidney problems were particularly susceptible to the effects of warfarin, and experienced higher rates of kidney decline than non-diabetic NVAF patients. The same was true for patients previously treated with warfarin. Also in these patients, Pradaxa treatment compared favourably to warfarin.
While the exact mechanism behind this difference has yet to be identified, there is a well-defined pathophysiological background. Vitamin K is known to protect against the build-up of calcium deposits in blood vessels, known as vascular calcification. Oral anticoagulation with vitamin K-antagonists such as warfarin, which block vitamin K in the body, have been associated with an increased rate of vascular calcification and vascular damage. Pradaxa is an oral direct thrombin inhibitor which does not interfere with vitamin K, but works in a different way to reduce blood clotting in order to protect patients with non-valvular atrial fibrillation against stroke.