Mechanical ventilation (MV) has been of great value in improving the survival of many patients suffering from respiratory failure. Although lifesaving in many patients, MV is associated with acute lung injury, termed ventilator-induced lung injury (VILI), and multiple organ failure including acute kidney injury (AKI). MV can triple the risk of in-hospital death in critically ill patients with AKI. MV exerts systemic hemodynamic effects through a complex interaction among intrathoracic pressure, intravascular volume, and cardiac performance. In addition, MV directly affects PaCO2 and PaO2 levels in patients. Mechanical stress caused by MV can affect cellular and molecular processes in the lung, a mechanism that has been called biotrauma. The biotrauma hypothesis consists of two pathways: first, mediators are released, and second, these mediators have biologic activity. Through effects on systemic hemodynamics MV can affect renal blood flow. Also effects on regulatory hormonal mechanisms may affect renal function, but more research is needed. Hypercapnia and severe hypoxemia resulting from or associated with MV have been found to correlate inversely with renal blood flow. Finally, an increasing number of mediators have been reported to increase in systemic circulation during MV and potentially may contribute to AKI. These mediators may exert their effect through several mechanisms: mediators can have effect on vasoactivity, inflammation, and apoptosis. In conclusion, MV is critical to survival in critically ill patients with effects on the kidney through several interacting mechanisms. This process is complicated further by the underlying disease.

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Keywords Biotrauma, Hypercapnia, Hypoxemia, Inflammatory mediators, Mechanical ventilation, Renal blood flow, Ventilator-induced lung injury
Persistent URL,
Kuiper, J.W. (Jan Willem), Groeneveld, A.B.J. (A.B. Johan), & Plötz, F.B. (2017). The Kidney During Mechanical Ventilation. doi:10.1016/B978-0-323-44942-7.00122-9