Key result
Platelets contribute to CV events in CKD by stimulating atherosclerotic lesions and thrombus formation.
Why the study?
Platelets play a dual role in hemostasis and cardiovascular event development, but the effects of chronic kidney disease on platelets and cardiovascular risk require clarification.
This review discusses the pathophysiological mechanisms by which platelets contribute to both hemostasis and cardiovascular events, with implications for cardiovascular risk in chronic kidney disease.
Platelet contributions to atherosclerosis may heighten CV risk in CKD; leaves open targeted therapies for prospective validation.
Platelets are crucial to prevent and stop bleeding, a process referred to as hemostasis. They do so by adhering to the damaged vascular wall, triggering platelet activation and the subsequent growth of a thrombus through an increasing accumulation of platelets and thrombin-generated fibrin. Platelets, however, also contribute to the occurrence of cardiovascular events by stimulating the formation and progression of atherosclerotic lesions and through their crucial involvement in the formation of thrombi triggered by vascular dysfunction, atherosclerotic plaque rupture, or plaque erosion.
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Baaten et al. (2022) conducted a review in Chronic Kidney Disease and Cardiovascular Risk. Chronic Kidney Disease was evaluated. Platelets contribute to cardiovascular events by stimulating atherosclerotic lesions and thrombus formation, with implications for cardiovascular risk in chronic kidney disease.
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