Abstract
We review the current literature on the molecular mechanisms involved in the pathogenesis of acute kidney injury induced by plasma mediators released by mechanical ventilation. A comprehensive literature search in the PubMed database was performed and articles were identified that showed increased plasma levels of mediators where the increase was solely attributable to mechanical ventilation. A subsequent search revealed articles delineating the potential effects of each mediator on the kidney or kidney cells. Limited research has focused specifically on the relationship between mechanical ventilation and acute kidney injury. Only a limited number of plasma mediators has been implicated in mechanical ventilation-associated acute kidney injury. The number of mediators released during mechanical ventilation is far greater and includes pro- and anti-inflammatory mediators, but also mediators involved in coagulation, fibrinolysis, cell adhesion, apoptosis and cell growth. The potential effects of these mediators is pleiotropic and include effects on inflammation, cell recruitment, adhesion and infiltration, apoptosis and necrosis, vasoactivity, cell proliferation, coagulation and fibrinolysis, transporter regulation, lipid metabolism and cell signaling. Most research has focused on inflammatory and chemotactic mediators. There is a great disparity of knowledge of potential effects on the kidney between different mediators. From a theoretical point of view, the systemic release of several mediators induced by mechanical ventilation may play an important role in the pathophysiology of acute kidney injury. However, evidence supporting a causal relationship is lacking for the studied mediators.
Highlights
Acute kidney injury (AKI) is a common problem in critically ill patients and carries significant morbidity and mortality
Despite advances in dialysis technology and supportive care, mortality resulting from AKI has remained unchanged over the past years and is as high as 80% when associated with respiratory insufficiency [1,2]
Mechanical ventilation (MV) is an independent risk factor for the development of AKI and can contribute to its development by three proposed mechanisms: blood gas disturbances leading to hypoxemia or hypercapnia and subsequent neurohumoral-mediated effects on renal blood flow during MV; changes in cardiac output, redistribution of intra-renal blood flow and stimulation of hormonal and sympathetic pathways may affect systemic and renal hemodynamics, thereby decreasing renal blood flow; and MV-induced biotrauma, defined as a pulmonary inflammatory reaction to MV with pulmonary mediator release [1,3]
Summary
Acute kidney injury (AKI) is a common problem in critically ill patients and carries significant morbidity and mortality. An observational study recently found that 75% of all patients with acute respiratory failure required some form of renal replacement therapy [1]. We review the current clinical and experimental literature describing mediators that are systemically released during MV and their effect on the kidney. We identify mediators whose release is attributable to MV and discuss the potential effects of these mediators on the kidney. This will provide a framework for future research on ventilation-induced renal injury through systemic mediator release
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