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Atypical Hemolytic Uremic Syndrome/Complement-Mediated Thrombotic Microangiopathy Triggered by SARS-CoV-2 Infection:
Malte Krakow1, Johanna H Hinrichs1, Judit Horvath2
1General Internal Medicine and Emergency Department, Nephrology, Hypertension and Rheumatology, University Hospital Münster, Münster, Germany.
Introduction:
Atypical hemolytic uremic syndrome (aHUS), commonly considered the prototypical form of complement-mediated thrombotic microangiopathy, is caused by dysregulated complement activation, often triggered by genetic mutations and external factors. We present a case of aHUS occurring 1 month after SARS-CoV-2 infection in a patient with a mutation in the complement factor H (CFH), a primary regulator of the alternative complement pathway.
Case Presentation:
A 41-year-old woman with no prior conditions developed acute kidney injury, hemolytic anemia, and thrombocytopenia 1 month after SARS-CoV-2 infection. Genetic testing identified a pathogenic CFH variant (c.3572C>T), and kidney biopsy confirmed thrombotic microangiopathy. Treatment with plasma exchange, corticosteroids, and C5 inhibitors led to remission of proteinuria and improved renal function within 2 months, avoiding dialysis. Even a second SARS-CoV-2 infection 6 months after the onset of aHUS and under continuous complement C5 inhibition did not result in further kidney damage.
Conclusions:
Our case report is consistent with observations made by several groups that SARS-CoV-2 infection may trigger aHUS in genetically predisposed individuals. Early diagnosis and complement-targeted therapy are crucial to prevent severe outcomes.
