title: Ischemic kidney injury and mechanisms of tissue repair.
abstract: Acute kidney injury (AKI) may result from ischemia or by the use of nephrotoxic agents. The incidence of AKI is variable, depends on comorbidities, and ranges from 5 to 35% in all hospitalized patients. The mechanisms of kidney injury exist within a large network of signaling pathways driven by interplay of inflammatory cytokines/chemokines, reactive oxygen species (ROS), and apoptotic factors. The effects and progression of injury overlap extensively with the remarkable ability of the kidney to repair itself both by intrinsic and extrinsic mechanisms that involve specific cell receptors/ligands as well as possible paracrine influences. The fact that kidney injury is usually part of a generalized comorbid condition makes it all the more challenging in terms of assessment of severity. In this review, we attempt to analyze the mechanisms of ischemic injury and repair in acute and chronic kidney disease from the perspectives of both preclinical and human studies.
authors.affiliation: Laboratory of Kidney Toxicology and Regeneration, Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institutes of Medicine, Boston, MA, USA.
authors.forename: Marwa
authors.initials: M
authors.lastname: El Sabbahy
authors.forename: Vishal S
authors.initials: VS
authors.lastname: Vaidya
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology* / Q000378:metabolism; D017209:Apoptosis; D006801:Humans; D007155:Immunologic Factors / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D007511:Ischemia / Q000150:complications / Q000378:metabolism*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism; D014945:Wound Healing
chemical_list: D007155:Immunologic Factors; D018836:Inflammation Mediators; D017382:Reactive Oxygen Species