Key result
Cardiorenal syndrome and heart failure progression are driven by complex bidirectional pathophysiological mechanisms involving neurohormonal activation, endothelial dysfunction, and oxidative stress.
This review highlights the complex pathophysiology of cardiorenal syndrome in heart failure, emphasizing the roles of oxidative stress and endothelial dysfunction as potential therapeutic targets.
Despite significant improvements in the treatment of virtually all cardiac disorders, heart failure (HF) is an exception, its prevalence is increasing, and only small extensions occur in survival. Several pathogenetic mechanisms appear to be operative in HF. These include higher overhead hemodynamic dysfunction associated with ventricular ischemia, remodeling with neurohumoral excessive stimulation, myocyte cycling abnormal calcium, inadequate or excessive proliferation of the extracellular matrix, accelerated apoptosis and genetic mutations. HF can present with reduced ejection fraction (EF), HFrEF, or with preserved EF (HFpEF). The interplay between diverse organ systems contributing to HF is mediated by the activation of counteracting neurohormonal pathways focused to re-establishing hemodynamic homeostasis. Cardiorenal Syndrome is a specific condition which is characterized by a rapid or chronic worsening of cardiac function leading to acute or chronic kidney injury (A/CKI) and /or the reciprocal organ dysfunction sequence can be possible. Even though its pathophysiology is complex and not still completely understood, oxidative stress and endothelial dysfunction seems to play a pivotal role. New Pathways between heart and kidney and its early recognition can also be targeted for more effective and beneficial HF treatments.
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Rosas-Peralta et al. (2016) conducted a review in Heart Failure and Cardiorenal Syndrome. Cardiorenal syndrome and heart failure progression are driven by complex bidirectional pathophysiological mechanisms involving neurohormonal activation, endothelial dysfunction, and oxidative stress.
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