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 bidirectional nature of 
the heart-kidney interactions, the classification of the CRS today includes 5 
subtypes whose etymology reflects the primary and secondary pathology, the time 
frame and simultaneous cardiac and renal codysfunction secondary to systemic 
disease. The CRS can generally be defined as a pathophysiological 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 
ischemia 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. The identification of patients and the pathophysiological 
mechanisms underlying each syndrome subtype will help to understand clinical 
derangements, to make the rationale for management strategies and to design 
future clinical trials with accurate selection and stratification of the studied 
population.