Heart and kidney are closely interacting organs which function interdependently. 
Organ crosstalk between these two organs is based on humoral regulation and by 
inflammatory mediators, which are similar to those dominating systemic 
inflammation syndrome. The close interaction between heart and kidney results in 
organ dysfunction following both chronic and acute functional impairment of the 
respective counterpart. These changes are summarized under the term cardiorenal 
syndrome (CRS) which is subdivided into 5 types. In the setting of emergency 
medicine and intensive care units, CRS types 1 and 3 are the most common. CRS 
type 1 is characterized by acute kidney injury (AKI) developing as a consequence 
of acute heart failure. CRS type 3 is represented by acute cardiac failure 
following AKI, often occurring as a consequence of nephrotoxins. Diagnosis of 
CRS should preferably be made on basis of the Kidney Disease: Improving Global 
Outcomes (KDIGO) criteria for the diagnosis and staging of AKI. The cardiac 
diagnostic workup should include echocardiography, electrocardiogram (ECG), 
cardiac enzymes, and brain natriuretic peptide (BNP). The therapeutic approach 
in CRS is primarily aimed at treating the causative organ dysfunction. In case 
of CRS type 3 this means ensuring adequate kidney perfusion, cautious fluid 
management, and avoiding additional nephrotoxins. In case of diuretic resistant 
fluid overload, early initiation of extracorporeal fluid removal, preferably by 
renal replacement therapy, should be considered.