Thrombozytenstörungen bei Urämie: Mediator von Herz- und Gefäßschäden

Patients with chronic kidney disease (CKD) have an increased risk of cardiovascular diseases (CVD) and thrombosis, with around half the patients with advanced CKD dying from CVD. Platelets not only play an essential physiological role in maintaining hemostasis but also contribute to CVD: they are key players in thrombus formation and the accompanying inflammatory reaction, contribute to atherosclerosis as the main cause of myocardial infarction and can also impact cardiac remodelling processes. Simultaneously, CKD patients suffer from an increased risk of thrombosis and bleeding, which highly complicates the antithrombotic treatment of CKD patients. The CKD patients, especially those with advanced CKD, were so far highly underrepresented in clinical trials of antithrombotic treatment, so that current clinical practice is mainly based on post hoc subgroup analyses of clinical trials and observational studies. Guidelines specifically optimized for this vulnerable patient group are so far unavailable. The platelet phenotype and function are altered in CKD patients, and a better understanding of the underlying mechanisms would support further improvement of antithrombotic treatment in CKD. This article discusses the role of platelets in CVD, the effect of CKD on platelets and the underlying mechanisms as well as current insights into and limitations of antithrombotic treatment of CKD patients.