The cardiorenal syndrome in human medicine: Pathophysiology, diagnosis and treatment

The cardiorenal syndrome (CRS) is characterized by an imbalance in the interaction between the heart and kidneys. This interaction usually provides a stable hemodynamic situation and organ function. In spite of multiple compensatory mechanisms, the dysfunction of one of the two organ systems is a risk factor for a dysfunction of the other. The underlying pathophysiological mechanisms of the deterioration of renal function in acute decompensated heart failure are probably associated with renal hypoperfusion due to decreased cardiac output and volume overload in the venous system, leading to a decreased renal blood flow and decreased renal autoregulation. The renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system and nitric oxide may in some circumstances contribute to the maintenance of renal function in heart failure, but on the other hand, they may also lead to a deterioration if there is an acute worsening of the heart failure. Early detection and treatment of CRS is important in treating renal impairment and cardiac dysfunction. Drugs which may affect the pathophysiological mechanisms of CRS might be useful for the recovery of renal function. Such treatments include diuretics, natriuretic peptides, ultrafiltration, inotropic agents and RAAS blockade. Despite these interventions, patients with CRS have an increased risk of morbidity and mortality.