Evolving practices in the management of acute kidney injury in the ICU (Intensive Care Unit)

Acute kidney injury (AKI) is a life-threatening illness whose mortality has remained high since the introduction of hemodialysis three decades ago. Current therapeutic options have been limited to dialytic support because there are no approved pharmacologics for the treatment of AKI. Previous clinical trials have focused on drugs and interventions that increase renal perfusion. These approaches have not been fruitful to date. However, early goal-directed therapy (EGDT) appears to improve renal and overall outcomes. The mechanism whereby EGDT improves outcomes appears to be related to decreased levels of proinflammatory cytokines and apoptosis. Inflammation and AKI are intimately related in preclinical studies. This relationship has been recently confirmed in clinical studies as well. Elevated concentrations of plasma IL-6 predict AKI in patients with sepsis, acute respiratory distress syndrome (ARDS), and hospital-acquired pneumonia. We postulate that inflammation causes AKI. This hypothesis could explain why clinical interventions focused on improving renal perfusion alone have not been effective. If inflammation causes AKI, than therapeutic interventions that decrease inflammation should improve renal outcome. Lung-protective strategies in patients with ARDS increase survival and decrease levels of proinflammatory cytokines. As expected, these decreased levels of proinflammatory cytokines as a result of implementing a lung-protective strategy are associated with improved renal outcome. Mounting evidence supports the hypothesis that inflammation is an important causal component of AKI. Interventions that safely decrease inflammation should be integrated in good clinical practice in order to maximize benefit. In the future, interventions and drugs targeted at inflammation may prove to be robust agents for the treatment of AKI.