Abstract
Progressive impairment of renal function can lead to uremia, which is associated with an increased risk of bleeding as well as thrombosis. Furthermore, many patients with chronic kidney disease (CKD) have an indication for an anticoagulation or antiplatelet therapy due to atrial fibrillation, coronary artery disease, thromboembolic disease, or peripheral artery disease. The treatment usually includes vitamin-K antagonists (VKAs) and/or platelet aggregation inhibitors. The direct oral anticoagulants (DOACs) inhibiting factor Xa or thrombin activity represent an alternative for heparins and VKAs. However, DOACs can further aggravate the bleeding risk in CKD patients. This is related to a combination of an accumulation of the substance due to the reduced renal clearance, an inhibition of thrombin-mediated platelet activation, and uremia associated factors such as impaired coagulation, platelet function, and platelet-vessel wall interactions. Furthermore, platelet aggregation inhibitors can also influence the bleeding risk, particularly if they are administered in combination with anticoagulants in patients with advanced CKD. In this review we discuss the different mechanisms leading to the increased risk of bleeding and thrombosis as well as the different options and problems related to an antiplatelet or anticoagulation therapy in CKD patients.
Keywords: Chronic kidney disease, anticoagulation, bleeding, thrombosis, direct oral anticoagulants, vitamin-K antagonists, platelet inhibitors.
Current Pharmaceutical Design
Title:Antiplatelet Agents and Anticoagulants in Patients with Chronic Kidney Disease - from Pathophysiology to Clinical Practice
Volume: 23 Issue: 9
Author(s): Jens Lutz*Kerstin Jurk
Affiliation:
- Section of Nephrology, I. Medizinische Klinik und Poliklinik, Universitätsmedizin Mainz, Langenbeckstr. 1, 55131 Mainz,Germany
Keywords: Chronic kidney disease, anticoagulation, bleeding, thrombosis, direct oral anticoagulants, vitamin-K antagonists, platelet inhibitors.
Abstract: Progressive impairment of renal function can lead to uremia, which is associated with an increased risk of bleeding as well as thrombosis. Furthermore, many patients with chronic kidney disease (CKD) have an indication for an anticoagulation or antiplatelet therapy due to atrial fibrillation, coronary artery disease, thromboembolic disease, or peripheral artery disease. The treatment usually includes vitamin-K antagonists (VKAs) and/or platelet aggregation inhibitors. The direct oral anticoagulants (DOACs) inhibiting factor Xa or thrombin activity represent an alternative for heparins and VKAs. However, DOACs can further aggravate the bleeding risk in CKD patients. This is related to a combination of an accumulation of the substance due to the reduced renal clearance, an inhibition of thrombin-mediated platelet activation, and uremia associated factors such as impaired coagulation, platelet function, and platelet-vessel wall interactions. Furthermore, platelet aggregation inhibitors can also influence the bleeding risk, particularly if they are administered in combination with anticoagulants in patients with advanced CKD. In this review we discuss the different mechanisms leading to the increased risk of bleeding and thrombosis as well as the different options and problems related to an antiplatelet or anticoagulation therapy in CKD patients.
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Cite this article as:
Lutz Jens*, Jurk Kerstin, Antiplatelet Agents and Anticoagulants in Patients with Chronic Kidney Disease - from Pathophysiology to Clinical Practice, Current Pharmaceutical Design 2017; 23 (9) . https://dx.doi.org/10.2174/1381612822666161205112156
DOI https://dx.doi.org/10.2174/1381612822666161205112156 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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