![]() ![]() Manuscripts can be submitted until the deadline. Once you are registered, click here to go to the submission form. Manuscripts should be submitted online at by registering and logging in to this website. This edition will focus on preclinical and clinical studies of the mechanisms causing AKI of different etiologies, novel biomarkers for the risk of AKI, and possible new therapies aimed at preventing or reversing AKI. Difficulty in treating AKI is compounded by the lack of biomarkers that detect the risk of AKI to allow preventative treatment. Although there have been significant advances in understanding the pathophysiology of AKI, there are no effective treatments to reverse AKI. The development of AKI therefore depends on different initiating causes, including impaired renal microcirculation, hypoxia, oxidative stress, and immune dysregulation. The pathophysiology of AKI is complex and differs depending on whether it is associated with, for example, sepsis, cardiopulmonary bypass, nephrotoxicity or ischemia reperfusion injury. It is now clear that AKI is not a single disease but an array of heterogeneous syndromes. Following AKI, there is an increased incidence of chronic kidney disease and conversion to end-stage renal disease. AKI is associated with a high morbidity and mortality and a greater risk of adverse outcomes after discharge. Acute kidney injury (AKI) is a major complication in patients admitted to hospital and in patients in intensive care units where incidence can reach 50%. ![]()
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