Abstract
Objective: The pathophysiology of the cardiorenal interaction remains poorly understood. We tested the hypothesis that renal insufficiency (RI) and cardiac dysfunction would contribute to the elevated sympathetic activity in patients with heart failure. Methods: In 79 patients with heart failure (ejection fraction (EF)<0.45), the resting muscle nerve sympathetic activity (MSNA), plasma norepinephrine (NE), brain natriuretic peptide (BNP) were determined. Estimated glomerular filtration rates (eGFR) less than 60 ml/min/1.73 m2 measured by simplified Modification of Diet in Renal Disease equation for Japanese was used to identify RI.
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