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Haemolytic uraemic syndrome associated with non shiga toxin-producing Escherichia coli bacteraemia: a case report

BACKGROUND: Haemolytic uraemic syndrome (HUS) is a thrombotic microangiopathy (TMA) characterized by predominant renal involvement. Several types of HUS can be distinguished: the most frequent « typical » HUS, due to shiga toxin producing Escherichia coli (STEC), “atypical” HUS due to complement alt...

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Detalles Bibliográficos
Autores principales: Bally, Stéphane, Fourcade, Jacques, Frémeaux-Bacchi, Véronique
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6505115/
https://www.ncbi.nlm.nih.gov/pubmed/31064333
http://dx.doi.org/10.1186/s12882-019-1357-3
Descripción
Sumario:BACKGROUND: Haemolytic uraemic syndrome (HUS) is a thrombotic microangiopathy (TMA) characterized by predominant renal involvement. Several types of HUS can be distinguished: the most frequent « typical » HUS, due to shiga toxin producing Escherichia coli (STEC), “atypical” HUS due to complement alternative pathway dysregulation and “secondary” HUS associated with various diseases/conditions, the classification of which is still subject to debate. CASE PRESENTATION: We report a case of HUS following E.coli prostatitis and bacteraemia in an adult male. He presented with severe renal and neurological involvement. Initially considered as a “typical” HUS, the condition was treated by antibiotics. No other specific treatment for HUS was administered. The outcome was favorable. We eventually identified a non shiga toxin producing E.coli. Genetic testing of the complement alternative pathway revealed a rare – potentially pathogenic – variant of factor H. This constitutes a possible factor of susceptibility for atypical HUS, suggesting that E.coli infection may be the trigger. CONCLUSION: This case raises the question of complement exploration for HUS associated with infections, in order to classify such cases of HUS in accordance with their underlying pathophysiological mechanisms.