Development and validation of a prediction tool for acute kidney injury in spontaneous Vs controlled ventilation patients with moderate to severe acute respiratory distress syndrome

AKI is a vexing clinical problem, as it is difficult to diagnose before there is a loss of organ function, which later becomes irreversible. Incidence of AKI in ARDS patients varies from 25-75%, and it contributes to high mortality among ARDS patients. Available therapies are mainly based on supportive measures and removal of nephrotoxic agents. Acute Respiratory Distress Syndrome (ARDS) is an inflammatory syndrome of the lung with a mortality rate of 35-65%. Mortality from Acute Lung Injury (ALI) and ARDS is approximately 40-50%. Since atelectasis and edema reduce aerated lung volumes in patients with ALI and ARDS, inspiratory airway pressures are often high, suggesting the presence of excessive distention or stretch of aerated lung. Ventilation-induced kidney injury (VIKI) is thought to occur due to changes in the hemodynamic pattern that impair renal perfusion, neurohumoral mediated alterations in intra-renal blood flow, and systemic inflammatory mediators generated by ventilator-induced lung injury. This could be the result of organ cross-talk during systemic inflammatory response. This presents clinicians with limited means to identify the optimal ventilator strategy for each patient. It is known that the ventilatory strategy could augment serum levels of inflammatory mediators due to alveolar stretch and endothelial injury. Still, there is a lack of understanding of its plasma concentration levels correlating with the development of VIKI. As a result, we aimed to develop and validate a prediction tool for acute kidney injury in spontaneous Vs controlled ventilation patients with moderate to severe acute respiratory distress syndrome.