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      Renal thrombotic microangiopathy caused by interferon beta-1a treatment for multiple sclerosis

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          Abstract

          Interferon beta-1a is available as an immunomodulating agent for relapsing forms of multiple sclerosis. Common side effects include flu-like symptoms, asthenia, anorexia, and administration site reaction. Kidney disorders are rarely reported. In this study we describe the case of a woman who has been undergoing treatment with interferon beta-1a for multiple sclerosis for 5 years. She developed a hemolytic-uremic syndrome with intravascular hemolysis in a context of severe hypertension. A kidney biopsy showed a thrombotic microangiopathy. This observation highlights an uncommon side effect of long-term interferon beta-1a therapy. Pathophysiological mechanisms leading to this complication might be explained by the antiangiogenic activity of interferon.

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          Most cited references 22

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          Atypical hemolytic-uremic syndrome.

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            Thrombotic microangiopathies.

             Joel L. Moake (2002)
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              The role of vascular endothelial growth factor (VEGF) in renal pathophysiology.

              Vascular endothelial growth factor (VEGF) is an endothelial-specific growth factor that promotes endothelial cell proliferation, differentiation and survival, mediates endothelium-dependent vasodilatation, induces microvascular hyperpermeability and participates in interstitial matrix remodeling. In the kidney, VEGF expression is most prominent in glomerular podocytes and in tubular epithelial cells, while VEGF receptors are mainly found on preglomerular, glomerular, and peritubular endothelial cells. The role of VEGF in normal renal physiology is essentially unknown. The absence of prominent effects of VEGF blockade in normal experimental animals suggests a limited function during homeostasis, although a role in the formation and maintenance of glomerular capillary endothelial fenestrations has been suggested. VEGF and its receptors are up-regulated in experimental animals and humans with type 1 and type 2 diabetes. Inhibition of VEGF has beneficial effects on diabetes-induced functional and structural alterations, suggesting a deleterious role for VEGF in the pathophysiology of diabetic nephropathy. VEGF is required for glomerular and tubular hypertrophy and proliferation in response to nephron reduction, and loss of VEGF is associated with the development of glomerulosclerosis and tubulointerstitial fibrosis in the remnant kidney. No firm conclusions on the role of VEGF in minimal change or membranous glomerulonephritis can be drawn. VEGF may be an essential mediator of glomerular recovery in proliferative glomerulonephritis. Glomerular and tubulointerstitial repair in thrombotic microangiopathy and cyclosporin nephrotoxicity may also be VEGF-dependent. In conclusion, VEGF is required for growth and proliferation of glomerular and peritubular endothelial cells. While deleterious in some, it may contribute to recovery in other forms of renal diseases.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Dove Medical Press
                1177-8881
                2013
                07 August 2013
                : 7
                : 723-728
                Affiliations
                [1 ]Clinical Pharmacology Department, Institute of Biology, University Hospital, Nantes, France
                [2 ]Clinical Nephrology and Immunology Department, University Hospital, Nantes, France
                [3 ]Laboratory of Pathology, University Hospital, Nantes, France
                [4 ]EA 4275 Biostatistics, Pharmacoepidemiology and Subjective Measures in Health Sciences, University of Nantes, Nantes, France
                Author notes
                Correspondence: Julien Mahe, Centre Régional de Pharmacovigilance, Service de Pharmacologie Clinique, Centre Hospitalier Universitaire de Nantes, 9 Quai Moncousu, 44093 Nantes Cedex, France, Tel +33 2 40 08 40 96, Fax +33 2 40 08 40 97, Email julien.mahe@ 123456chu-nantes.fr
                Article
                dddt-7-723
                10.2147/DDDT.S42138
                3741076
                23950639
                © 2013 Mahe et al, publisher and licensee Dove Medical Press Ltd

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

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                Case Report

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