Year: 2008
Type: article
Abstract: The glomerular microvasculature is particularly susceptible to injury in thrombotic microangiopathy, but the mechanisms by which this occurs are unclear. We report the cases of six patients who were treated with bevacizumab, a humanized monoclonal antibody against vascular endothelial growth factor (VEGF), in whom glomerular disease characteristic of thrombotic microangiopathy developed. To show that local reduction of VEGF within the kidney is sufficient to trigger the pathogenesis of thrombotic microangiopathy, we used conditional gene targeting to delete VEGF from renal podocytes in adult mice; this resulted in a profound thrombotic glomerular injury. These observations provide evidence that glomerular injury in patients who are treated with bevacizumab is probably due to direct targeting of VEGF by antiangiogenic therapy.
Source: New England Journal of Medicine
Authors: Vera Eremina, J. Ashley Jefferson, Jolanta Kowalewska, Howard Hochster, Mark Haas, Joseph Weisstuch, Catherine Richardson, Jeffrey B. Kopp, M. Golam Kabir, Peter H. Backx, Hans-Peter Gerber, Napoleone Ferrara, Laura Barisoni, Charles E. Alpers, Susan E. Quaggin
Institutions: Mount Sinai Hospital, Mount Sinai Hospital, University of Toronto, Lunenfeld-Tanenbaum Research Institute, University of Washington, New York University, Johns Hopkins University, Johns Hopkins Medicine, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Toronto General Hospital Research Institute, Seagen (United States), Genentech, St. Michael's Hospital
Language: English
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W2028031291