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• W1552020886 abstract "Ischemic injury to the kidney is the most common cause of acute kidney injury. Despite intensive basic research and in critical care for decades it is still associated with high mortality rates of ~50% in the intensive care unit. It is observed in a variety of clinical situations such as cardiac arrest with recovery, organ transplantation, or heminephrectomy. Postischemic acute kidney injury is characterized by an abrupt decrease in glomerular filtration rate (GFR) (the hallmark feature of acute kidney injury), and increased renal vascular resistance that determines a persistent reduction in renal blood flow (RBF) and tubular injury. However, the pathophysiological mechanisms responsible for the postischemic renal injury and the profoundly depressed renal function remain incompletely understood. The accumulated data in the literature are compatible with the hypothesis that ischemic acute kidney injury is essentially a phenomenon of altered renal hemodynamics linked critically to endothelial cell dysfunction caused by the production of high levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS), leading to decreased nitric oxide availability as a consequence of its destruction to form peroxynitrite, associated with an intracellular energy store depletion. The oxidative and nitrosative stress will produce lipid peroxidation, oxidative DNA damage and modification and inactivation of proteins that originates an inflammatory reaction characterized by endothelial activation and injury, enhanced endothelial cell-leukocyte adhesion, leukocyte entrapment, and a reduction in microvascular blood flow mainly affecting the renal outer medulla as indicated by the marked vascular congestion typically observed in this zone of the kidney. On the other hand, and depending on the severity of renal ischemia, tubular epithelial cells will undergo a varying degree of necrosis or apoptosis with tubular obstruction followed by both an 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. Because of the importance of endothelial cells in this process, emphasis will be placed on the involvement of oxidative and nitrosative stress in causing endothelial dysfunction, the sources of oxygen and nitrogen reactive species, and the interactions between them, specially superoxide anion and nitric oxide because together they form peroxynitrite, a potent oxidant and nitrosant agent. Among other factors, the severity of acute kidney injury is mainly determined by the duration of the ischemia. Special attention will be paid to the vascular and hemodynamic" @default.
• W1552020886 created "2016-06-24" @default.
• W1552020886 creator A5011180004 @default.
• W1552020886 creator A5021965333 @default.
• W1552020886 creator A5032691811 @default.
• W1552020886 creator A5081161893 @default.
• W1552020886 date "2012-05-23" @default.
• W1552020886 modified "2023-10-14" @default.
• W1552020886 title "Oxidative and Nitrosative Stress in the Ischemic Acute Renal Failure" @default.
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