Exploration of the pathophysiological mechanisms underlying hemodialysis associated cardiac ischemic injury
Abstract
Hemodialysis (HD) provides life-saving treatment in individuals with kidney failure. However, HD is associated with poor quality of life and extremely high mortality rates mainly caused by cardiovascular disease due to heart failure and sudden cardiac death. Standard pharmacological treatment developed within the non-kidney disease community are largely ineffective in HD patients because of the difference in pathophysiology of cardiovascular mortality. HD treatment causes hypotension and recurrent ischemic injury to multiple vascular beds including the heart, leading to heart failure. These injuries can be abrogated by improving the patient’s tolerability of the treatment. To apply interventions that may improve hemodynamic tolerability of HD, it is crucial to understand the mechanisms of HD-induced injury at every layer of the vasculature: the endothelial, microvasculature and macrovasculature. The purpose of this thesis was to study the endothelial and vascular dysfunction effecting tissue perfusion as a result of HD and under conditions of intradialytic exercise and alteration of dialysate sodium concentration.