# Atypical Hemolytic Uremic Syndrome Triggered by COVID‐19 Infection in a Pediatric Patient With CD46 Mutation

## TL;DR

A child with a CD46 gene mutation developed a rare blood disorder after a COVID-19 infection, showing the need for early diagnosis and targeted treatment.

## Contribution

This case is the first to report aHUS triggered by COVID-19 in a pediatric patient with a CD46 mutation.

## Key findings

- The patient showed aHUS symptoms one week after viral symptoms during the pandemic.
- A homozygous CD46 mutation was identified through genetic testing.
- Eculizumab therapy was required after relapse despite initial treatment.

## Abstract

Atypical hemolytic uremic syndrome (aHUS) is a rare form of thrombotic microangiopathy (TMA) that is considered life‐threatening and caused by dysregulation of the complement system. Here, we report a previously healthy 8‐year‐old boy who presented with features of aHUS 1 week after viral symptoms during the COVID‐19 pandemic. The patient was initially admitted for viral symptoms, pallor, edema, and urine color changes. Laboratory tests revealed anemia, thrombocytopenia, and elevated levels of creatinine and blood urea nitrogen (BUN). Despite fluid and electrolyte management, he developed pulmonary edema, necessitating hemodialysis and plasmapheresis. Genetic testing identified a homozygous pathogenic mutation in the CD46 gene, which encodes membrane cofactor protein (MCP). While initially responding to treatment, the patient experienced a relapse, requiring further interventions including eculizumab therapy. This case highlights the potential of COVID‐19 to trigger complement‐mediated TMA and emphasizes the importance of prompt diagnosis, genetic assessment, and targeted complement inhibition in managing aHUS.