Abstract:

Cardiorenal syndrome may partly be due to high venous pressure, rather than traditional mechanisms involving low cardiac output. Proposed pathophysiologic mechanisms include reduced transglomerular pressure, elevated renal interstitial pressure, myogenic and neural reflexes, baroreceptor stimulation, activation of sympathetic nervous and renin angiotensin aldosterone systems, and enhanced proinflammatory pathways. Although the kidney improvements observed in trials using traditional pharmacologic strategies or ultrafiltration have been attributed to improvement in cardiac output and renal perfusion, based on the physiology there is reason to hypothesize that there were benefits from reducing renal venous pressure.