Acute kidney injury (AKI) presents a significant challenge in the management of critically ill patients, as it is associated with increased mortality, prolonged hospital stays, and increased healthcare costs. In certain conditions, such as during sepsis or after cardiac surgery, AKI is one of the most frequent complications, affecting 30%-50% of patients. Over time, even after the resolution of AKI, it can evolve into chronic kidney disease, a leading global cause of mortality, and cardiovascular complications. Despite significant improvement in the care of critically ill patients over the past two decades, the incidence of AKI remains stable, and novel approaches aiming at reducing its occurrence or improving AKI outcomes are still mostly lacking. However, recent insights into the pathophysiology of AKI within critical care settings have shed light on new pathways for both prevention and treatment, providing various new therapeutic targets aimed to mitigating kidney injury. These advancements highlight the intricate and multifaceted nature of the mechanisms underlying AKI, which could explain the challenge of identifying an effective treatment. Among these targets, modulation of the inflammatory responses and the cellular metabolism, hemodynamic regulation and enhancement of cellular repair mechanisms, have emerged as promising options. These multifaceted approaches offer renewed hope for limiting the incidence and severity of AKI in critically ill patients. Several ongoing clinical trials are evaluating the efficacy of these different strategies and we are facing an exiting time with multiple therapeutic interventions being tested to prevent or treat AKI. In this review, we aim to provide a summary of the new drugs evaluated for preventing or treating AKI in critical care and surgical settings.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763585 | PMC |
http://dx.doi.org/10.1016/j.jointm.2024.08.001 | DOI Listing |
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