BMC nephrology · 2019
Haemolytic uraemic syndrome associated with non shiga toxin-producing Escherichia coli bacteraemia: a case report.
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Bally Stéphane, Fourcade Jacques, Frémeaux-Bacchi Véronique
Аннотация
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.
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.