Pathological changes in the heart or kidney can instigate the release of a cascade of cardiorenal mediators that promote injury in the other organ. Combined dysfunction of heart and kidney is referred to as cardiorenal syndrome (CRS) and has gained considerable attention. CRS has been classified into five distinct entities, each with different major pathophysiological changes. Despite the magnitude of the public health problem of CRS, the underlying mechanisms are incompletely understood, and effective intervention is unavailable. Animal models have allowed us to discover pathogenic molecular changes to clarify the pathophysiological mechanisms responsible for heart-kidney interactions and to enable more accurate risk stratification and effective intervention. Here, this article focuses on the use of currently available animal models to elucidate mechanistic insights in the clinical cardiorenal phenotype arising from primary cardiac injury, primary renal disease with special emphasis of chronic kidney disease-specific risk factors, and simultaneous cardiorenal/renocardiac dysfunction. The development of novel animal models that recapitulate more closely the cardiorenal phenotype in a clinical scenario and discover the molecular basis of this condition will be of great benefit.
Keywords: acute heart failure; acute kidney injury; animal models; cardiorenal syndrome; chronic heart failure; chronic kidney disease.