1. The impact of cold ischemia time on renal transplant outcome
Claudio E. Ponticelli 
Kidney International 
Volume 87, Issue 2, Pages (February 2015)
DOI: /ki
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2. Figure 1
Ischemia of the renal tissue causes anaerobic glycolysis, reduced generation of ATP, and increased production of reactive oxygen species (ROS). As a result, there is intracellular accumulation of lactic acid, malfunction of the Na/K ATPase enzyme, and oxidative stress that can cause pathological and functional tissue damage. The blood reperfusion of the injured tissue triggers a paradoxical response with increased generation of ROS, chemokines, and polymorphonuclear leukocytes (PMNs). The cell consequences of ischemia–reperfusion injury may be mild or severe. Endothelial cells and tubular epithelial cells are particularly vulnerable, and their injury may lead to delayed graft function (DGF). It may repair without consequences or may result in progressive renal insufficiency. Apart from these effects, the ischemia–reperfusion injury may cause release of cytosolic or intranuclear proteins from dying cells. The molecular patterns of these substances are recognized as danger signals by the receptors of the innate immune system that activate inflammatory cells and mediators. The inflammation may worsen the tissue damage and may stimulate dendritic cells (DCs) to become mature. Mature DCs intercept the tissue antigen and migrate to the lymphatic system, where they present the antigen (Ag) to T cells, activating the adaptive immune system and favoring an increased immune reactivity against the transplanted kidney.
Kidney International  , DOI: ( /ki )
Copyright © 2015 International Society of Nephrology Terms and Conditions