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Herz und Diabetes

Thrombozytenfunktion und antithrombozytäre Therapie bei chronischer Nierenerkrankung

Heart and diabetes

Platelet function and antiplatelet therapy in chronic kidney disease

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Zusammenfassung

Patienten mit einer chronischen Nierenerkrankung (CKD) haben ein erhöhtes Thromboserisiko, und etwa 50 % dieser Patienten mit fortgeschrittener Nierenerkrankung versterben durch eine kardiovaskuläre Erkrankung. Parallel zum erhöhten Thromboserisiko haben Patienten mit CKD – insbesondere bei fortgeschrittener CKD – ein erhöhtes Blutungsrisiko, welches parallel zur Verschlechterung der Nierenfunktion zunimmt. Durch diesen parallel bestehenden prohämorrhagischen/prothrombotischen Phänotyp ist die antithrombozytäre Therapie im Alltag schwierig, und Daten zeigen, dass CKD-Patienten mit akutem Koronarsyndrom (ACS) weniger häufig einer leitliniengerechten Therapie zugeführt werden. Die zugrunde liegenden Mechanismen sind zum jetzigen Zeitpunkt unzureichend verstanden, und sowohl thrombozytenabhängige als auch -unabhängige Mechanismen werden diskutiert. Entsprechend gibt es keine spezifische Therapie oder Therapiestrategien für Patienten mit CKD. Zudem sind CKD-Patienten in den Registrierungsstudien zur antithrombozytären Therapie unterrepräsentiert, und für Patienten mit fortgeschrittener CKD (CKD ≥ 4) gibt es keine Daten aus randomisierten Studien. Aktuelle Leitlinienempfehlungen beruhen somit auf Subgruppenanalysen und Observationsstudien. Zudem bleiben Fragen zur Dauer der Therapie, zu Risikoscores zur Abschätzung des Blutungsrisikos und zum potenziellen Nutzen von Deeskalierungs- und Eskalierungsstrategien unbeantwortet und sollten in Zukunft verstärkt in den Fokus genommen werden.

Abstract

Patients with chronic kidney disease (CKD) have an increased risk of thrombosis and approximately 50% of patients with advanced CKD die because of a cardiovascular disease. In addition to an increased risk of thrombosis, patients with CKD and particularly with advanced CKD, have an increased risk of hemorrhage, which increases parallel to the decline of kidney function. Due to this parallel existence of the prohemorrhagic and prothrombotic phenotype, antiplatelet treatment is difficult in the daily routine and data show that CKD patients with acute coronary syndrome (ACS) are less likely to receive guideline-conform treatment. The underlying mechanisms are currently insufficiently understood and both platelet-dependent mechanisms and also platelet-independent mechanisms are under discussion. Accordingly, there is currently no specific treatment or treatment strategy for patients with CKD. In addition, CKD patients are underrepresented in registration studies on antiplatelet treatment and there are no data from randomized trials for patients with advanced CKD (CKD ≥ 4). Current guideline recommendations are therefore based on subgroup analyses and observational studies. In addition, questions on the duration of treatment, on risk scores for estimation of the risk of hemorrhage and on potential benefits of escalation and de-escalation strategies remain largely unanswered and should therefore be the focus of future studies.

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Correspondence to Martin Berger.

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M. Berger, C.C.F.M.J. Baaten, H. Noels, N. Marx und K. Schütt geben an, dass kein Interessenkonflikt besteht.

Für diesen Beitrag wurden von den Autoren keine Studien an Menschen oder Tieren durchgeführt. Für die aufgeführten Studien gelten die jeweils dort angegebenen ethischen Richtlinien.

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Berger, M., Baaten, C.C.F.M.J., Noels, H. et al. Herz und Diabetes. Herz 47, 426–433 (2022). https://doi.org/10.1007/s00059-022-05129-3

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