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Abstract: SA-PO221

A Rare Case of Clostridium Difficile Causing Atypical Hemolytic Uremic Syndrome

Session Information

  • Trainee Case Reports - V
    October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 1202 Glomerular Diseases: Immunology and Inflammation


  • Carter, Jessamyn, University of Oklahoma School of Community Medicine, Tulsa, Oklahoma, United States
  • Regmi, Narottam, University of Oklahoma School of Community Medicine, Tulsa, Oklahoma, United States

Atypical hemolytic uremic syndrome (aHUS) is a rare form of thrombotic microangiopathy mediated by excess activation or dysregulation of the alternate complement pathway. The incidence is 2 per 1 million people in the United States. We present a case of aHUS caused by C. difficile with persistent renal failure.

Case Description

52-year-old morbidly obese man with hypertension, sleep apnea, and recurrent deep vein thrombosis admitted for worsening fatigue and bloody diarrhea since treatment with clindamycin then trimethoprim-sulfamethoxazole 2 weeks prior. He had acute renal failure with creatinine 4.9 and oliguria, hemolytic anemia, thrombocytopenia, leukocytosis, and active urine sediment with RBCs, WBCs and protein. CT abdomen and renal ultrasound were unremarkable. Left renal biopsy showed severe acute glomerular microangiopathic injury. He began intermittent hemodialysis (HD) and plasma exchange. ADAMTS13, total complement, C3/C4, ANA and ANCA and tests for E.coli 0157:H7, Shiga toxin, HIV, and hepatitis were normal. aHUS genotype panel was equivocal. Stool was positive for C. difficile.
After plasma exchange and steroids, he remained oliguric on HD. Eculizumab was started for aHUS. Despite treatment, he remains HD dependent awaiting transplant.


90% of HUS is secondary, usually to E.coli 0157:H7 or Shiga toxin (typical diarrhea+ HUS), S. pneumoniae infection, pregnancy, or drugs. There is no known causation by clindamycin or trimethoprim-sulfamethoxazole. Normal complement and equivocal aHUS genotype results do not rule out aHUS. A few case reports suggest C. difficile infection may cause HUS, though prior cases had full renal recovery. Our patient’s clinical, lab, and histopathologic findings support diagnosis of aHUS from C. difficile infection.
Though rare, C. difficile must be considered as a cause of aHUS. Our patient presents further difficulty as renal function remains poor despite antibiotic therapy and eculizumab.

Biopsy with cortical necrosis, severe acute glomerular microangiopathy