Pulmonary hypertension (PH) comprises a group of clinical and pathophysiologic entities with similar characteristics due to a variety of associated conditions. Chronic kidney disease is one of these causes, but the pathogenesis of PH in this population is still unknown. HP has been associated with poor survival in hemodialysis patients. However, data on the prevalence and the influence of other factors which can affect the survival of patients with PH with end-stage kidney disease are limited. Endothelial dysfunction, increased platelet activation and aggregation, activation of the coagulation system and reduction of endogenous anticoagulants are some of the homeostatic mechanisms that might be associated with both chronic kidney disease and venous thromboembolism (VTE), and they has been hardly studied in each one of these situation. Nevertheless, little is known regarding the possible association between chronic kidney disease, VTE and platelet aggregation. It has been proved that thromboembolic events arising from platelet hyperaggregability may increase the risk of cardiovascular disease (CVD) in patients with chronic kidney disease. Our group has shown association among PH and volume overload, hypoalbuminemia, and inflammatory biomarkers in hemodialysis patients. We hypothesize that platelet hyperaggregability, endothelial dysfunction, and thromboembolic pulmonary disease are involved in the pathogenesis of PH in chronic kidney disease. We also hypothesize that the phenomenon of platelet hyperaggregability may be present in this population.
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