Abstract
The development of simultaneous decompensation in cardiac and renal function is a common phenomenon in patients with congestive heart failure. Termed the cardiorenal syndrome (CRS), this joint deterioration in cardiac output and renal filtration is the result of a complex interplay of hemodynamic and neurohormonal factors. Recently, endothelial dysfunction, inflammation and uremia have been recognized as contributors to the crosstalk responsible for the development of CRS. Management strategies for the treatment of CRS involve correction of hemodynamic derangements and regulation of neurohormonal pathways. Future therapies may target more newly recognized components of CRS pathophysiologic development.
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