Type 3 CRS is characterized by an abrupt and primary worsening of kidney function (e.g., AKI, ischemia, or glomerulonephritis), leading to acute cardiac dysfunction (e.g., HF, arrhythmia, ischemia). Type 3 CRS appears less common than type 1 CRS, but this may only be due to the fact that, unlike type 1 CRS, it has not been systematically studied. AKI is a growing disorder in hospital and ICU patients. When the RIFLE (risk, injury, and failure; loss; and end-stage kidney disease) consensus definition is used, AKI has been identified in close to 9% of hospital patients (64). In a large ICU database, AKI was observed in more than 35% of patients (65). Acute kidney injury can affect the heart through several pathways (Figure 3), whose hierarchy is not yet established. Fluid overload can contribute to the development of pulmonary edema. Hyperkalemia can contribute to arrhythmias and may cause cardiac arrest. Untreated uremia affects myocardial contractility through the accumulation of myocardial depressant factors (66) and pericarditis (67). Acidemia produces pulmonary vasoconstriction (68), which can significantly contribute to right-sided HF. Acidemia appears to have a negative inotropic effect (69) and might, together with electrolyte imbalances, contribute to an increased risk of arrhythmias (70). Finally, renal ischemia itself may precipitate activation of inflammation and apoptosis at cardiac level (9).