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Abstract Cardiorenal syndrome can be generally defined as a pathophysiologic disorder of the heart and kidneys, whereby acute or chronic dysfunction of one organ may induce acute or chronic dysfunction of the other. The coexistence of kidney and heart failure carries an extremely bad prognosis. A new classification of the CRS with 5 subtypes has been presented. Type 1 CRS reflects an abrupt worsening of cardiac function leading to acute kidney injury. Type 2 CRS comprises chronic abnormalities in cardiac function causing progressive chronic kidney disease. Type 3 CRS consists of an abrupt worsening of renal function causing acute cardiac dysfunction. Type 4 CRS describes a state of chronic kidney disease contributing to decreased cardiac function, cardiac hypertrophy, and/or increased risk of adverse cardiovascular events. Type 5 CRS reflects a systemic condition (e.g., sepsis) causing both cardiac and renal dysfunction. Interactions between inflammation, the renin-angiotensin system, the balance between the nitric oxide and reactive oxygen species and the sympathetic nervous system form the cardiorenal connectors and are cornerstonesin the pathophysiology of CRS. For management, drugs that impair kidney function are undesirable, particularly in a population with already compromised or at-risk kidney function. In severe volume-loaded patients who are refractory to diuretics, management of cardiorenal dysfunction is challenging. New therapeutic avenues involving nesiritide, vasopressin antagonists, adenosine antagonists, endothelin antagonists and ultrafiltration are being investigated. In the absence of underlying primary renal parenchymal disease, mechanical ventricular assist devices or cardiac transplantation achieve reversal of the progressive cardiorenal syndrome. Thus, treatment decisions must be based on a combination of patient’s condition and understanding of individual treatment options. |