Extracellular vesicles as mediators of vascular inflammation in kidney disease

doi:10.5527/wjn.v5.i2.125

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Mar 6, 2016 (publication date) through Feb 23, 2026

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World Journal of Nephrology

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2220-6124

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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Review

World J Nephrol. Mar 6, 2016; 5(2): 125-138
Published online Mar 6, 2016. doi: 10.5527/wjn.v5.i2.125

Extracellular vesicles as mediators of vascular inflammation in kidney disease

Alexandra Helmke, Sibylle von Vietinghoff

Alexandra Helmke, Sibylle von Vietinghoff, Division of Nephrology and Hypertension, Hannover Medical School, D-30625 Hannover, Germany

Author contributions: Both authors contributed to all aspects of manuscript preparation.

Conflict-of-interest statement: We have no conflicts of interest regarding this work.

Correspondence to: Dr. med. Sibylle von Vietinghoff, Division of Nephrology and Hypertension, Hannover Medical School, Carl-Neuberg-Strasse 1, D-30625 Hannover, Germany. vonvietinghoff.sibylle@mh-hannover.de

Telephone: +49-0511-60060412 Fax: +49-0511-60060435

Received: August 28, 2015
Peer-review started: September 2, 2015
First decision: November 27, 2015
Revised: December 18, 2015
Accepted: January 8, 2016
Article in press: January 11, 2016
Published online: March 6, 2016
Processing time: 186 Days and 1.4 Hours

Core Tip

Core tip: This review addresses the role of extracellular vesicles (EVs) in vascular inflammation that can cause renal damage and is also shaped by uremic mediators. Vasculitides are common causes of renal damage. Functionally, neutrophil EVs induced by anti-neutrophil cytoplasmic antibody contribute to endothelial damage. EVs are main distributors of shiga toxin in the circulation and into tissues in typical hemolytic uremic syndrome. In atherosclerosis in patients with and without kidney disease, endothelial EVs are elevated. Uremic EVs are deficient in mediating vascular relaxation. EVs modulate mononuclear phagocyte differentiation, cytokine production, lipid phagocytosis and antigen presentation, atherosclerotic inflammatory processes significantly altered in uremia.