• Journal title: Universal Journal of Pharmaceutical Research
• ISSN: 2456-8058 (online)
• Publisher: UJPR
• Country of publisher: india
• Date added to EuroPub: 2019/Feb/24

• LCC Subject Category: Medicine
• Publisher's keywords: remote organ injury, Renal ischemia, reperfusion injury reactive oxygen species (ROS), inflammatory response
• Language of fulltext: english
• Full-text formats available: PDF

Asmaa A. Khalifa, Mai El-Sayed Ghoneim

• Double blind peer review
• Editorial Board
• Aims and scope
• Instructions for authors
• Time From Submission to Publication: 13

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Because of the high rate of baseline oxygen use by renal cells, kidney is highly influenced by obstruction of arterial blood inflow and subsequent shortage of the received oxygen, this condition is known as Ischemic injury. There are many clinical settings associated with unavoidable ischemic state such as kidney transplantation, partial nephrectomy or suprarenal procedures of the aorta. During ischemia many cellular changes occur including vascular congestion and adhesion of inflammatory cells to the endothelium with subsequent infiltration into the kidney tissue. Following ischemia, a phase known as Reperfusion begins and involves a return of blood and oxygen supply to micro vessels. Reperfusion was expected to restore the damage occurred during the ischemic phase, paradoxically, reperfusion leads to more congestion, red cells trapping and excessive generation of reactive oxygen species (ROS), which can oxidatively modify significantly every type of biomolecule, thereby inducing cell dysfunction and induce reperfusion injury. Ischemia reperfusion injury (IRI) is also related to a phenomenon called Remote Organ Injury (ROI) in which the damaging effect induced by I/R is not only restricted to the tissue that undergoing the initial ischemia but also it leads to injury to remote organs such as the liver, lung, gut. ROI usually occurs by the same mechanisms seen in the local injury induced by I/R including the generation of ROS, leukocytes, and inflammatory mediators (e.g; TNF-α). These substances are directly released from the primary injured tissue or indirectly from activated leukocytes or other inflammatory cells causing organ dysfunctions in distant organs.