title: Reactive oxygen and nitrogen species in the renal ischemia/reperfusion injury.
abstract: Renal ischemia is the most common cause of acute kidney injury (AKI) still associated with high mortality rates of about 50% in the intensive care unit. Postischemic AKI is characterized by decreased glomerular filtration rate and high renal vascular resistance with endothelial activation and dysfunction, a process of critical importance that is followed by a reduction in microvascular blood flow mainly affecting the renal outer medulla. The pathophysiology of postischemic AKI remains incompletely understood, although it seems to be a phenomenon of altered renal hemodynamics, linked critically to the production of high amounts of nitric oxide and free radicals. On the other hand, and depending on the severity of renal ischemia, tubular epithelial cells undergo a varying degree of necrosis or apoptosis with tubular obstruction followed by both, anatomical and functional recovery. The way in which vascular and tubular epithelium recover determines the final status of the renal function, ranging from full recovery to chronic renal failure and ultimately to end-stage renal disease. In this review we will revise the mechanisms responsible for these pathophysiologic alterations, including the role of heme oxygenase system and sex differences in the susceptibility to ischemic acute renal failure, and we will also review the pre- and postconditioning phenomena, in which brief episodes of ischemia before (pre-conditioning) or after (post-conditioning) the prolonged ischemia have a protective effect on AKI after reperfusion. Interestingly, these protective responses can be elicited by ischemizing distant tissues (remote conditioning). A better understanding of these mechanisms may help to improve the clinical outcome of those patients.
authors.affiliation: Department of Physiology, School of Medicine, University of Murcia, 30100. Campus Universitario de Espinardo, Murcia, Spain.
authors.forename: Francisca
authors.initials: F
authors.lastname: Rodriguez
authors.forename: Barbara
authors.initials: B
authors.lastname: Bonacasa
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Fenoy
authors.forename: Miguel G
authors.initials: MG
authors.lastname: Salom
mesh_terms: D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D006801:Humans; D007668:Kidney / Q000098:blood supply*; D009569:Nitric Oxide / Q000502:physiology*; D026361:Reactive Nitrogen Species / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015427:Reperfusion Injury / Q000201:enzymology / Q000378:metabolism*
chemical_list: D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D006419:Heme Oxygenase (Decyclizing)