We propose cardiorenal syndrome (CRS), excessive cardiovascular and renal mortality and morbidity when either organ is diseased, to be a consequence of excessive central sympathetic activity impacting both organs. Congestion, the several cardiac manifestations of the CRS, including hypertrophy, systolic and diastolic dysfunction, and tachyarrhythmias and both the functional and anatomic deterioration of renal function seen in the CRS are logically attributed to excessive chronic sympathetic activity. Thus, reduction of sympathetic activity, either by selective organ denervation, systemic pharmacologic blockade or reduction of chemosensitivity are logical strategies for the treatment or prevention of CRS.