In asymptomatic patients with left ventricular dysfunction, an inability to excrete a volume load precedes any evidence of diminution in cardiac output ( 6). At the late stage of heart failure, the cardiorenal syndrome has been attributed to a postulated further decrease in cardiac output during aggressive diuresis to relieve symptoms.Īlthough internally consistent, this conception is dissolving. This reduction is followed by a postulated subsequent progression of cardiac dysfunction that further diminishes cardiac output, impairing renal blood flow, and further activating responses that decrease renal function but fail to normalize cardiac output. Worsening indices of renal function limit symptomatic and neurohormonal therapy, lead to longer hospital stay, and predict higher rate of early rehospitalization and death.Ī classic conception of the cardiorenal interaction in heart failure progression begins with a postulated early reduction in cardiac output that stimulates systemic and intrarenal responses to retain fluid and restores cardiac output at new circulating volume.

Risk increases with longer history of heart failure and high chronic diuretic doses. Originally described in patients with low ejection fraction, this syndrome is now recognized to occur as often in patients admitted with heart failure and preserved ejection fraction, many of whom have hypertension ( 5), diabetes, and impaired baseline renal function.

An elevation in creatinine of 0.3 mg/dl or proportional rises of 25% during diuresis are observed in more than 20% of heart failure hospitalizations ( 4). The cardiorenal syndrome can be defined narrowly as worsening renal function limiting diuresis despite obvious clinical volume overload ( 3). Changing view of cardiorenal connections during disease progression

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