Abstract
The central venous pressure (CVP) is traditionally used as a surrogate of intravascular volume. CVP measurements therefore are often applied at the bedside to guide fluid administration in postoperative and critically ill patients. Pursuing high CVP levels has recently been challenged. A high CVP might impede venous return to the heart and disturb microcirculatory blood flow which may cause tissue congestion and organ failure. By imposing an increased "afterload" on the kidney, an elevated CVP will particularly harm kidney hemodynamics and promote acute kidney injury (AKI) even in the absence of volume overload. Maintaining the lowest possible CVP should become routine to prevent and treat AKI, especially when associated with septic shock, cardiac surgery, mechanical ventilation, and intra-abdominal hypertension.