Thrombotic microangiopathy due to acquired ADAMTS13 deficiency in a patient receiving interferon-beta treatment for multiple sclerosis

Int Urol Nephrol. 2014 Jan;46(1):239-42. doi: 10.1007/s11255-013-0401-7. Epub 2013 Feb 24.

Abstract

Thrombotic microangiopathies (TMAs) can be due to inherited or acquired ADAMTS13 deficiency. Acquired deficiency is mainly associated with autoantibodies directed to ADAMTS13, including drug-induced forms. A few cases of TMA have been reported in association with interferon-alpha treatment and more rarely with interferon-beta. We report the case of a 52-year-old male with TMA-associated severe renal failure secondary to severe ADAMTS13 deficiency due to an anti-ADAMTS13 IgG antibody which developed after interferon-beta treatment for multiple sclerosis. Treatment included interferon-beta discontinuation, immediate plasma exchange therapy, corticosteroids, and hemodialysis. After an initial hematologic improvement, early hemolysis relapse led us to introduce rituximab allowing durable hematologic recovery. This is the first reported case of interferon-beta-induced TMA due to acquired ADAMTS13 deficiency that was treated by rituximab.

Publication types

  • Case Reports

MeSH terms

  • ADAM Proteins / deficiency*
  • ADAMTS13 Protein
  • Acute Kidney Injury / etiology
  • Antibodies, Monoclonal, Murine-Derived / therapeutic use*
  • Humans
  • Immunologic Factors / adverse effects*
  • Immunologic Factors / therapeutic use
  • Interferon-beta / adverse effects*
  • Male
  • Middle Aged
  • Multiple Sclerosis / drug therapy
  • Protein Deficiency / chemically induced*
  • Protein Deficiency / drug therapy
  • Rituximab
  • Thrombosis / chemically induced*
  • Thrombosis / drug therapy

Substances

  • Antibodies, Monoclonal, Murine-Derived
  • Immunologic Factors
  • Rituximab
  • Interferon-beta
  • ADAM Proteins
  • ADAMTS13 Protein
  • ADAMTS13 protein, human