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Abstract: PO1551

A Case of Thrombotic Microangiopathy from an Intra-Abdominal Abscess

Session Information

Category: Glomerular Diseases

  • 1203 Glomerular Diseases: Clinical, Outcomes, and Trials

Authors

  • Prakash-Polet, Sindhuri, Columbia University Irving Medical Center, New York, New York, United States
  • Nahapetyan, Lusine, Columbia University Irving Medical Center, New York, New York, United States
  • Rosen, Raphael Judah, Columbia University Irving Medical Center, New York, New York, United States
  • Kudose, Satoru, Columbia University Irving Medical Center, New York, New York, United States
  • Crew, Russell J., Columbia University Irving Medical Center, New York, New York, United States
Introduction

Infection mediated thrombotic microangiopathy (TMA) has a high mortality with many patients requiring kidney replacement therapy. Recognition of TMA can be difficult in the setting of sepsis as clinical abnormalities can overlap. We report a case of TMA from complicated diverticulitis and polymicrobial intra-abdominal abscess.

Case Description

A 25 year old non-vegetarian man presented with generalized abdominal pain, fatigue, chills and intermittent epistaxis. He was found to have severe acute renal failure with Coombs positive hemolytic anemia, thrombocytopenia, high fibrinogen, high PT/PTT, low ADAMTS13 activity (15%) and ADAMTS13 inhibitor. Further workup showed sigmoid diverticulitis with a large intra-abdominal and small intrahepatic abscess which was culture positive for Streptococcus anginosus (an oral microbe with proclivity to abscess formation) and Escherichia coli. Shiga toxin was not tested. Kidney biopsy revealed acute TMA. Drainage of the abscess and treatment with antibiotics resolved the systemic features of TMA. Renal recovery was protracted and the patient required dialysis for three months, with a last sCr of ~2mg/dl.

Discussion

Infection mediated TMA is an important third subgroup of thrombotic microangiopathy. The mechanism of injury is likely due to the concerted effort of both bacteria. E.coli produced shiga toxin causes direct damage to the endothelial cells, worsened by the incorporation of non-human sialic acid from dairy and meat, increasing toxin affinity to endothelial cells and injury. S.anginosus produces an exotoxin that can lyse erythrocytes and platelets allowing IgM binding to the exposed Tn antigen, leading to the coombs positivity observed. There is decreased hepatic synthesis of ADAMTS13 in sepsis, and ADAMTS13 autoantibodies are reported in Ecoli mediated TMA. Given high fatality rate, prompt recognition and treatment of the underlying infection is pivotal as ongoing infection propagates microangiopathy. Severe features of TMA can develop during the clinical course necessitating intensive treatments such as plasmapheresis. As infection can be a frequent trigger of TMA among patients with complement abnormalities, patients should undergo genetic testing of the regulatory genes involved in the complement system.