Maintenance of blood volume, vascular tone, and hemodynamic stability depends on a set of elegant interactions between the heart and kidney. For some time, physicians have recognized that severe dysfunction in either of these organs seldom occurs in isolation. However, only recently have we attempted to define and apply the widespread concept of the cardiorenal syndrome (CRS). Despite our growing use of the term, there is still some debate as to its true definition. More important, the process itself remains enigmatic; our understanding of the complex physiological, biochemical, and hormonal derangements that encompass the CRS is woefully deficient and may lead to improper medical management of patients.
Because renal dysfunction portends such a dismal prognosis in cardiac failure and vice versa, there has been a recent surge of interest in identifying precise pathophysiological connections between the failing heart and kidneys. Understanding the mechanisms involved in the CRS will allow us to target therapies that interrupt this dangerous feedback cycle.
In 2004, a working group of investigators at the National Heart, Lung, and Blood Institute defined the CRS as a state in which therapy to relieve heart failure (HF) symptoms is limited by further worsening renal function.1 Although this definition is succinct and understandable and probably reflects the most common use of the term, some authors argue that it is simplistic to the point of being inaccurate.2 Several groups have recently proposed that the definition of CRS be broadened in an attempt to stress the complex and bidirectional nature of pathophysiological interactions between the failing heart and kidneys. That is, each dysfunctional organ has the ability to initiate and perpetuate disease in the other organ through common hemodynamic, neurohormonal, and immunologic/biochemical feedback pathways.
Proper use of the term CRS should correct a common misunderstanding: that kidney dysfunction in HF …