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Updated: Feb 15, 2026

Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
Published on: August 9, 2013
Paradigms of acute kidney injury in the intensive care setting
John A Kellum1, John R Prowle2,3
1Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh School of Medicine and University of Pittsburgh Medical Center, 3347 Forbes Avenue, Suite 220, Pittsburgh, Pennsylvania 15213, USA.
Abstract:
Acute kidney injury (AKI) is a heterogeneous clinical syndrome that has multiple aetiologies, variable pathogenesis and diverse outcomes. However, these heterogeneities are not reflected in current approaches to the diagnosis and, to some degree, treatment of AKI. For example, congestive heart failure and dehydration can produce identical changes in serum creatinine level and urine output (parameters that are used to define AKI); however, they differ vastly in their physiological contexts and demand completely opposite treatments. AKI is often still considered to be a homogeneous clinical entity, which implies a uniform pathogenesis and a well-defined prognosis. As a consequence, efforts to find effective AKI treatments have been hampered by a lack of clear clinical classifications for various types of AKI. In addition, subclassification of AKI into subclinical phenotypes - for example, on the basis of protein biomarkers and other in vitro diagnostics that take into account disease aetiology and underlying pathogenesis - might be necessary to develop therapeutic approaches that effectively target the widely differing pathomechanisms of AKI. In this Review, we discuss the major subtypes of AKI that are associated with sepsis, major surgery, renal hypoperfusion and nephrotoxin exposure -situations that are typically seen in the intensive care setting. We consider differences and similarities in their phenotype, pathogenesis and outcomes and how this information might be used to guide treatment.
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