The term cardiorenal syndrome (CRS) has increasingly been used in recent years 
without a constant meaning and a well accepted definition. To include the vast 
array of interrelated derangements, and to stress the bi-directional nature of 
the heart-kidney interactions, the classification of the cardiorenal syndrome 
includes today five sub-types whose etymology reflects the primary and secondary 
pathology, the time-frame and simultaneous cardiac and renal co-dysfunction 
secondary to systemic disease. The cardiorenal syndrome can be generally defined 
as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic 
dysfunction in one organ may induce acute or chronic dysfunction in the other 
organ. Type I CRS reflects an abrupt worsening of cardiac function (e.g. acute 
cardiogenic shock or decompensated congestive heart failure) leading to acute 
kidney injury. Type II CRS describes chronic abnormalities in cardiac function 
(e.g. chronic congestive heart failure) causing progressive and permanent 
chronic kidney disease. Type III CRS consists in an abrupt worsening of renal 
function (e.g. acute kidney ischaemia or glomerulonephritis) causing acute 
cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type IV CRS 
describes a state of chronic kidney disease (e.g. chronic glomerular disease) 
contributing to decreased cardiac function, cardiac hypertrophy and/or increased 
risk of adverse cardiovascular events. Type V CRS reflects a systemic condition 
(e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. 
Biomarkers can help to characterize the subtypes of the CRS and to indicate 
treatment initiation and effectiveness.