Shiga Toxin as a Potential Trigger of CFHR1 Deletion-Associated Thrombotic Microangiopathy

Swarna S. Nalluru, Meera Sridharan, Ronald S. Go, Samar Said, Ariela L. Marshall

Research output: Contribution to journalReview articlepeer-review

5 Scopus citations

Abstract

Thrombotic microangiopathy (TMA) may result from a variety of clinical conditions, including thrombotic thrombocytopenic purpura, Shiga toxin-producing Escherichia coli-associated hemolytic uremic syndrome and complement-mediated hemolytic uremic syndrome. Thrombocytopenic purpura is diagnosed when ADAMTS13 is <10%, while a diagnosis of Shiga toxin-producing Escherichia coli-associated hemolytic uremic syndrome is made with the evidence of infection by Shiga toxin-producing Escherichia coli. Diagnosis of complement-mediated hemolytic uremic syndrome is not dependent on a specific laboratory test and is a diagnosis of exclusion. TMA is a rare disease and finding individuals that have more than 1 concurrent etiology leading to TMA is even more rare. Here we describe the presentation and management of an individual with CFHR1 deletion-associated TMA also found to have a positive stool Shiga toxin. We discuss the significance of Shiga toxin in serving as a trigger for development of TMA in an individual predisposed to development of TMA due to presence of a homozygous deletion in CFHR1.

Original languageEnglish (US)
Pages (from-to)492-498
Number of pages7
JournalAmerican Journal of the Medical Sciences
Volume356
Issue number5
DOIs
StatePublished - Nov 2018
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2018 Southern Society for Clinical Investigation

Keywords

  • Complement
  • Eculizumab
  • Hemolytic uremic syndrome
  • Shiga toxin
  • Thrombotic microangiopathy

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