Abstract: TH-PO206

Parvovirus Infection Mimicking Atypical Hemolytic Uremic Syndrome in an Immunocompetent Adult

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports

Authors

  • Shovlin, Gerald, Geisinger Medical Center, Danville, Pennsylvania, United States
  • Kleman, Mark A., Geisinger Health System, Danville, Pennsylvania, United States
  • Vadakara, Joseph, Geisinger Medical Center, Danville, Pennsylvania, United States
  • Mallampalli, Syam Prasad, Geisinger Medical Center, Danville, Pennsylvania, United States
  • bermudez, maria, Geisinger Medical Center, Danville, Pennsylvania, United States
Background

Human parvovirus B19 (PB19) has been associated with thrombotic microangiopathies (TMA) including hemolytic uremic syndrome (HUS) both in immunocompetent and immunosuppressed individuals. To our knowledge, specific pathophysiologic mechanisms for this association is unclear. We present a case of acute PB19 infection presenting as atypical HUS and discuss potential pitfalls in the diagnosis and implications for therapy.

Methods

A 20-year-old female presents with anuric AKI, thrombocytopenia, and MAHA (low haptoglobin, presence of schistocytes and high LD 1500). Autoimmune diseases including lupus, antiphospholipid syndrome and cryoglobulinemia were ruled out. Her mono test, hepatitis panel, and HIV were negative. C3 complement level was low at 78. Bone marrow biopsy showed reactive neutrophilia and occasional RBC fragments. ADAMTS13 and alternate complement studies were sent and patient was started on dialysis and plasmapheresis (PLEX) for presumed diagnosis of HUS. Reticulocyte count was inappropriately normal for which PB19 PCR was checked and found to be > 600,000 copies. ADAMTS13 came back normal so the patient was started on Eculuzimab (900 mg weekly for 4 doses, then 1200 mg every two weeks) for possible atypical HUS. Alternate complement pathway (TMA functional panel) returned normal, without identifiable mutations predisposing the patient to aHUS. She completely recovered, came off dialysis, and Eculizumab was discontinued.

Conclusion

Our patient presented with features of atypical HUS in the setting of acute PB19 infection. Her ADAMTS13 and alternate complement pathway were normal making the exact pathophysiologic mechanism of this association unclear. Prompt search for PB19 as a potential trigger of her clinical picture and rapid initiation of PLEX appeared to favor her rapid improvement. Potential role of Eculizumab remains unclear but likely prudent until alternate pathway studies are available. Further studies to better understand this association and approach to therapy are mandated.