The role of platelets in acute kidney injury

Acute kidney injury (AKI), a major public health problem associated with high mortality and increased risk of progression towards end-stage renal disease, is characterized by the activation of intra-renal haemostatic and inflammatory processes. Platelets, which are present in high numbers in the cir...

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Veröffentlicht in:	Nature reviews. Nephrology Jg. 14; H. 7; S. 457 - 471
Hauptverfasser:	Jansen, Marcel P B, Florquin, Sandrine, Roelofs, Joris J T H
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	England Nature Publishing Group 01.07.2018
Schlagworte:	Acute Kidney Injury - drug therapy Acute Kidney Injury - etiology Acute Kidney Injury - physiopathology Animals Blood Platelets - metabolism Blood Platelets - physiology Cell Communication Complement System Proteins - metabolism Cyclooxygenase Inhibitors - therapeutic use Cytokines - metabolism Endothelium, Vascular - metabolism Hemodynamics Humans Inflammation Inflammation - blood Kidneys Leukocytes - metabolism Phosphodiesterase 3 Inhibitors - therapeutic use Platelet Activation Platelet Aggregation Inhibitors - therapeutic use Platelet Glycoprotein GPIIb-IIIa Complex - antagonists & inhibitors Purinergic P2Y Receptor Antagonists - therapeutic use Renal Circulation
ISSN:	1759-5061, 1759-507X, 1759-507X
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Abstract	Acute kidney injury (AKI), a major public health problem associated with high mortality and increased risk of progression towards end-stage renal disease, is characterized by the activation of intra-renal haemostatic and inflammatory processes. Platelets, which are present in high numbers in the circulation and can rapidly release a broad spectrum of bioactive mediators, are important acute modulators of inflammation and haemostasis, as they are the first cells to arrive at sites of acute injury, where they interact with endothelial cells and leukocytes. Diminished control of platelet reactivity by endothelial cells and/or an increased release of platelet-activating mediators can lead to uncontrolled platelet activation in AKI. As increased platelet sequestration and increased expression levels of the markers P-selectin, thromboxane A , CC-chemokine ligand 5 and platelet factor 4 on platelets have been reported in kidneys following AKI, platelet activation likely plays a part in AKI pathology. Results from animal models and some clinical studies highlight the potential of antiplatelet therapies in the preservation of renal function in the context of AKI, but as current strategies also affect other cell types and non-platelet-derived mediators, additional studies are required to further elucidate the extent of platelet contribution to the pathology of AKI and to determine the best therapeutic approach by which to specifically target related pathogenic pathways.
AbstractList	Acute kidney injury (AKI), a major public health problem associated with high mortality and increased risk of progression towards end-stage renal disease, is characterized by the activation of intra-renal haemostatic and inflammatory processes. Platelets, which are present in high numbers in the circulation and can rapidly release a broad spectrum of bioactive mediators, are important acute modulators of inflammation and haemostasis, as they are the first cells to arrive at sites of acute injury, where they interact with endothelial cells and leukocytes. Diminished control of platelet reactivity by endothelial cells and/or an increased release of platelet-activating mediators can lead to uncontrolled platelet activation in AKI. As increased platelet sequestration and increased expression levels of the markers P-selectin, thromboxane A2, CC-chemokine ligand 5 and platelet factor 4 on platelets have been reported in kidneys following AKI, platelet activation likely plays a part in AKI pathology. Results from animal models and some clinical studies highlight the potential of antiplatelet therapies in the preservation of renal function in the context of AKI, but as current strategies also affect other cell types and non-platelet-derived mediators, additional studies are required to further elucidate the extent of platelet contribution to the pathology of AKI and to determine the best therapeutic approach by which to specifically target related pathogenic pathways.Acute kidney injury (AKI), a major public health problem associated with high mortality and increased risk of progression towards end-stage renal disease, is characterized by the activation of intra-renal haemostatic and inflammatory processes. Platelets, which are present in high numbers in the circulation and can rapidly release a broad spectrum of bioactive mediators, are important acute modulators of inflammation and haemostasis, as they are the first cells to arrive at sites of acute injury, where they interact with endothelial cells and leukocytes. Diminished control of platelet reactivity by endothelial cells and/or an increased release of platelet-activating mediators can lead to uncontrolled platelet activation in AKI. As increased platelet sequestration and increased expression levels of the markers P-selectin, thromboxane A2, CC-chemokine ligand 5 and platelet factor 4 on platelets have been reported in kidneys following AKI, platelet activation likely plays a part in AKI pathology. Results from animal models and some clinical studies highlight the potential of antiplatelet therapies in the preservation of renal function in the context of AKI, but as current strategies also affect other cell types and non-platelet-derived mediators, additional studies are required to further elucidate the extent of platelet contribution to the pathology of AKI and to determine the best therapeutic approach by which to specifically target related pathogenic pathways. Acute kidney injury (AKI), a major public health problem associated with high mortality and increased risk of progression towards end-stage renal disease, is characterized by the activation of intra-renal haemostatic and inflammatory processes. Platelets, which are present in high numbers in the circulation and can rapidly release a broad spectrum of bioactive mediators, are important acute modulators of inflammation and haemostasis, as they are the first cells to arrive at sites of acute injury, where they interact with endothelial cells and leukocytes. Diminished control of platelet reactivity by endothelial cells and/or an increased release of platelet-activating mediators can lead to uncontrolled platelet activation in AKI. As increased platelet sequestration and increased expression levels of the markers P-selectin, thromboxane A2, CC-chemokine ligand 5 and platelet factor 4 on platelets have been reported in kidneys following AKI, platelet activation likely plays a part in AKI pathology. Results from animal models and some clinical studies highlight the potential of antiplatelet therapies in the preservation of renal function in the context of AKI, but as current strategies also affect other cell types and non-platelet-derived mediators, additional studies are required to further elucidate the extent of platelet contribution to the pathology of AKI and to determine the best therapeutic approach by which to specifically target related pathogenic pathways. Acute kidney injury (AKI), a major public health problem associated with high mortality and increased risk of progression towards end-stage renal disease, is characterized by the activation of intra-renal haemostatic and inflammatory processes. Platelets, which are present in high numbers in the circulation and can rapidly release a broad spectrum of bioactive mediators, are important acute modulators of inflammation and haemostasis, as they are the first cells to arrive at sites of acute injury, where they interact with endothelial cells and leukocytes. Diminished control of platelet reactivity by endothelial cells and/or an increased release of platelet-activating mediators can lead to uncontrolled platelet activation in AKI. As increased platelet sequestration and increased expression levels of the markers P-selectin, thromboxane A , CC-chemokine ligand 5 and platelet factor 4 on platelets have been reported in kidneys following AKI, platelet activation likely plays a part in AKI pathology. Results from animal models and some clinical studies highlight the potential of antiplatelet therapies in the preservation of renal function in the context of AKI, but as current strategies also affect other cell types and non-platelet-derived mediators, additional studies are required to further elucidate the extent of platelet contribution to the pathology of AKI and to determine the best therapeutic approach by which to specifically target related pathogenic pathways.
Author	Roelofs, Joris J T H Jansen, Marcel P B Florquin, Sandrine
Author_xml	– sequence: 1 givenname: Marcel P B surname: Jansen fullname: Jansen, Marcel P B organization: Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands – sequence: 2 givenname: Sandrine surname: Florquin fullname: Florquin, Sandrine organization: Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands – sequence: 3 givenname: Joris J T H surname: Roelofs fullname: Roelofs, Joris J T H email: j.j.roelofs@amc.nl organization: Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands. j.j.roelofs@amc.nl
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Snippet	Acute kidney injury (AKI), a major public health problem associated with high mortality and increased risk of progression towards end-stage renal disease, is...
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SubjectTerms	Acute Kidney Injury - drug therapy Acute Kidney Injury - etiology Acute Kidney Injury - physiopathology Animals Blood Platelets - metabolism Blood Platelets - physiology Cell Communication Complement System Proteins - metabolism Cyclooxygenase Inhibitors - therapeutic use Cytokines - metabolism Endothelium, Vascular - metabolism Hemodynamics Humans Inflammation Inflammation - blood Kidneys Leukocytes - metabolism Phosphodiesterase 3 Inhibitors - therapeutic use Platelet Activation Platelet Aggregation Inhibitors - therapeutic use Platelet Glycoprotein GPIIb-IIIa Complex - antagonists & inhibitors Purinergic P2Y Receptor Antagonists - therapeutic use Renal Circulation
Title	The role of platelets in acute kidney injury
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