ABSTRACT
INTRODUCTION The term “cardiorenal syndrome” often refers to a condition in which renal impairment occurs as a result of cardiac dysfunction (1). This view has been supported by the observation that a previously impaired renal function normalizes after a cardiac assist device is implanted in a patient with end-stage heart failure (HF) (2). The expression “cardiorenal syndrome” has also been used to describe the negative effects of renal disorders on heart structure and function (3). Thus, although the term “cardiorenal syndrome” is loosely applied to many pathologic interactions between the heart and the kidney, a comprehensive defi nition is lacking. To be inclusive of the damage/dysfunction produced in either the heart or the kidney by an acute or chronic disease of the other organ, the cardiorenal syndrome should be classifi ed according to whether the impairment of each organ is primary, secondary or whether abnormal heart and kidney functions occur simultaneously as a result of a systemic disease (4). For example, acute HF decompensation can cause both acute renal injury and chronic kidney disease: a decreased cardiac output is associated with renal arterial underfi lling and increased venous pressure which, in turn, result in a reduced glomerular fi ltration rate (GFR) (3). Activation of the renin−angiotensin−aldosterone system (RAAS), initially aimed at restoring GFR, eventually leads to increased renal expression of endothelin-1 (ET-1), a potent proinfl ammatory and profi brotic vasoconstrictor peptide known to mediate acute and chronic kidney injury (4).
