Published Paper Details:

A substantial percentage of deaths in individuals with chronic kidney disease (CKD) are attributable to cardiovascular disease (CVD), which is the primary cause of morbidity and mortality in this population. Endothelial dysfunction, oxidative stress, chronic inflammation, and an elevated prothrombotic state are some of the intricate processes that interact between CKD and CVD. These factors increase the likelihood of arterial calcification and atherosclerotic events, which are exacerbated by conventional CVD risk factors such diabetes, hypertension, and dyslipidemia, which are commonly seen in individuals with chronic kidney disease. For patients with established atherosclerotic disease and those at high cardiovascular risk, antiplatelet therapy--specifically, aspirin and clopidogrel--is essential for lowering thrombotic consequences. Aspirin, an irreversible inhibitor of cyclooxygenase-1 (COX-1), reduces platelet aggregation by blocking the formation of thromboxane A2. Clopidogrel, an inhibitor of the P2Y12 receptor, stops platelets from activating and aggregating when ADP is present. Both medications have shown effective in the general population, but because of their changed pharmacokinetics, elevated risk of bleeding, and greater vulnerability to side effects, using them in CKD patients poses special difficulties[1]