Type I interferon causes thrombotic microangiopathy by a dose-dependent toxic effect on the microvasculature

Author:

Kavanagh David1,McGlasson Sarah2ORCID,Jury Alexa2,Williams Jac3,Scolding Neil4,Bellamy Chris5,Gunther Claudia6,Ritchie Diane3,Gale Daniel P.7,Kanwar Yashpal S.8,Challis Rachel1,Buist Holly9,Overell James10,Weller Belinda3,Flossmann Oliver11,Blunden Mark12,Meyer Eric P.13,Krucker Thomas14,Evans Stephen J. W.15,Campbell Iain L.16,Jackson Andrew P.2,Chandran Siddharthan3,Hunt David P. J.23ORCID

Affiliation:

1. National Renal Complement Therapeutics Centre, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom;

2. Medical Research Council Institute of Genetics and Molecular Medicine and

3. Centre for Clinical Brain Sciences, Edinburgh University, Edinburgh, United Kingdom;

4. Institute of Clinical Neurosciences, University of Bristol, Bristol, United Kingdom;

5. Department of Renal Medicine, University of Edinburgh, Edinburgh, United Kingdom;

6. Department of Dermatology, University Hospital, Technical University Dresden, Dresden, Germany;

7. Centre for Nephrology, Royal Free Hospital, University College London, London, United Kingdom;

8. Feinberg School of Medicine, Northwestern University, Chicago, IL;

9. Department of Cellular Pathology, Royal Victoria Hospital, Newcastle upon Tyne, United Kingdom;

10. Institute of Neurological Sciences, Glasgow University, Glasgow, United Kingdom;

11. Royal Berkshire Hospital, Reading, United Kingdom;

12. Barts and the London National Health Service Trust, London, United Kingdom;

13. Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland;

14. The Scripps Research Institute, La Jolla, CA;

15. London School of Hygiene & Tropical Medicine, London, United Kingdom; and

16. School of Molecular Bioscience, University of Sydney, Sydney, Australia

Abstract

Key Points Type I IFN therapies can cause a dose-dependent TMA. Recombinant type I IFN therapies should be stopped at the earliest opportunity in patients who develop TMA.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Reference43 articles.

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