Abstract
Acute kidney injury (AKI), defined as an abrupt increase in serum creatinine, a reduced urinary output, or both, is experiencing considerable evolution in terms of our understanding of the pathophysiological mechanisms and its impact on other organs. Oxidative stress and reactive oxygen species (ROS) are main contributors to organ dysfunction in AKI, but they are not alone. The precise mechanisms behind multi-organ dysfunction are not yet fully accounted for. The building up of uremic toxins specific to AKI might be a plausible explanation for these disturbances. However, controversies have arisen around their effects in organs other than the kidney, because animal models usually depict AKI as a kidney-specific injury. Meanwhile, humans present AKI frequently in association with multi-organ failure (MOF). Until now, medium-molecular-weight molecules, such as inflammatory cytokines, have been proven to play a role in endothelial and epithelial injury, leading to increased permeability and capillary leakage, mainly in pulmonary and intestinal tissues.
Highlights
Acute kidney injury (AKI) is defined as a rapid increase in serum creatinine, a reduced urinary output, or both
The clinical associations and pathogenesis of AKI are complex, it is frequently encountered in critical patients and may have several contributing factors, including reduced blood flow, nephrotoxic exposure and systemic inflammatory response
There is a growing body of evidence surrounding the organ-specific effects of certain uremic toxins, which may be involved in organ cross-talk and mediate damage and recovery
Summary
AKI is defined as a rapid increase in serum creatinine, a reduced urinary output, or both. A diverse range of uremic toxins has been identified, some of which have an impact on cardiovascular mortality in patients with chronic kidney disease (CKD) in pre-dialysis care Their effects in AKI remain controversial [4] and could represent a likely explanation for organ failure in AKI [5]. An initial insult (hypoxia, IRI, hypovolemia, etc.) may cause organ failure, with AKI being one of the consequences; this does not exclude a potential role for individual toxins aggravating distant organ failure These conditions may increase production of toxins, which accumulate in the setting of decreased urinary clearance, making it difficult to conduct studies regarding the effects of any given uremic toxin in a specific organ [9]. Given the high burden of complications in these settings, research is needed to provide possible therapeutic targets and guide clinicians in order to improve patient outcomes
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