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. 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. 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.