Meningococcemia in a Boy with Dense Deposit Disease Receiving the C5 Complement Inhibitor Ravulizumab: A Case Report

Dense deposit disease, also known as C3 glomerulopathy, is a rare renal disorder caused by abnormal complement deposition in the glomerular basement membrane. Patients often require long-term immunosuppressive therapy and, in some cases, complement inhibitors such as ravulizumab. While effective at limiting renal damage, complement blockade significantly increases susceptibility to invasive infections from encapsulated bacteria, particularly Neisseria meningitidis. Despite immunization and antimicrobial prophylaxis, these patients remain incompletely protected. We describe a case of meningococcemia in a fully vaccinated adolescent with dense deposit disease on ravulizumab therapy.

A 17-year-old male with a history of dense deposit disease on mycophenolate mofetil and ravulizumab presented to the pediatric emergency department with fever, vomiting, altered mental status, and a rapidly evolving petechial-purpuric rash. He was fully immunized with both meningococcal conjugate and serogroup B vaccines. Initial evaluation revealed fever, hypotension, and altered level of consciousness. Laboratory studies showed leukocytosis, elevated inflammatory markers, and blood cultures subsequently confirmed N. meningitidis. Empiric ceftriaxone and vancomycin were initiated, later narrowed to ceftriaxone. Supportive management included intravenous (IV) fluids, vasopressors, IV immunoglobulin, and dexamethasone. The patient demonstrated rapid improvement, with resolution of hemodynamic instability and normalization of kidney function. He was discharged on hospital day eight with prophylactic penicillin and close outpatient follow-up.

This case underscores the risk associated with complement inhibition, even in fully vaccinated individuals. Clinicians must maintain high vigilance for meningococcal disease in immunocompromised patients and initiate early aggressive therapy to optimize outcomes.