Journal of Medical Cases, ISSN 1923-4155 print, 1923-4163 online, Open Access
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Case Report

Volume 16, Number 7, July 2025, pages 254-258

Influenza A H1N1 Triggering Complement-Mediated Hemolytic Uremic Syndrome

Figure

↓  Figure 1. Patient’s oncologic treatment timeline. CM-HUS: complement-mediated hemolytic uremic syndrome; PR: partial response; GI: gastrointestinal; auto-HSCT: autologous hematopoietic stem cell transplantation; CAR-T: chimeric antigen receptor T-cell therapy.
Figure 1.

Table

↓  Table 1. Etiologies of Complement-Mediated Thrombotic Microangiopathies
 
Etiology Mechanism
HIV: human immunodeficiency virus.
Genetic mutations in complement regulators: (e.g., CFH, CFI, MCP/CD46, C3, CFB) Lead to loss of control over the alternative complement pathway, resulting in excessive complement activation, endothelial injury, and microvascular thrombosis
Acquired autoantibodies (e.g., anti-factor H) Autoantibodies inhibit function of complement regulatory proteins, causing unrestrained complement activation and endothelial damage
Pregnancy Increased complement activation triggering disease
Infections (e.g., influenza, HIV) Trigger for complement overactivation
Surgery or trauma Systemic inflammation and complement activation
Certain medications (e.g., calcineurin inhibitors) Drug-induced endothelial injury
Transplantation Immunological stress and complement activation