The clinical syndrome congestive heart failure (CHF) has its origins rooted in a salt-avid state mediated largely by effector hormones of the renin-angiotensin-aldosterone system. In recent years, this cardiorenal perspective of CHF has taken on a broader perspective. One which focuses on a progressive systemic illness, whose major features include the presence of oxidative stress in diverse tissues and elevated circulating levels of proinflammatory cytokines coupled with a wasting of soft tissues and bone.
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