New insights into the pathophysiological mechanisms underlying cardiorenal syndrome

Abstract

Communication between the heart and kidney occurs through various bidirectional pathways. The heart maintains continuous blood flow through the kidney while the kidney regulates blood volume thereby allowing the heart to pump effectively. Cardiorenal syndrome (CRS) is a pathologic condition in which acute or chronic dysfunction of the heart or kidney induces acute or chronic dysfunction of the other organ. CRS type 3 (CRS-3) is defined as acute kidney injury (AKI)-mediated cardiac dysfunction. AKI is common among critically ill patients and correlates with increased mortality and morbidity. Acute cardiac dysfunction has been observed in over 50% of patients with severe AKI and results in poorer clinical outcomes than heart or renal dysfunction alone. In this review, we describe the pathophysiological mechanisms responsible for AKI-induced cardiac dysfunction. Additionally, we discuss current approaches in the management of patients with CRS-3 and the development of targeted therapeutics. Finally, we summarize current challenges in diagnosing mild cardiac dysfunction following AKI and in understanding CRS-3 etiology.