Atypical haemolytic uraemic syndrome. Two cases

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Ana Terra Morena Queiroz
Hemilanna Hadassa Silva Matozinho
Maria do Rosário Ferraz Roberti

Resumo

Haemolytic uraemic syndrome is a disfunction known as thrombotic microangiopathy. When it is not caused by Shiga toxin, produced by Escherichia coli, the disease is called atypical, which is classified in primary and secondary. This paper aims to study two case reports diagnosed as atypical haemolytic uraemic syndrome secondary to calcineurin inhibitors. Both are patients that had undergone kidney transplantation, but lost their graft due to atypical haemolytic uraemic syndrome. Their presentations were pancytopenia for one and anaemia of difficult management for the other, the first one was taking the medication called tacrolimus and the second one was taking cyclosporine. Nephrotoxicity related to the usage of calcineurin inhibitors was already known since it was introduced in the medical practice, however its efficacy in the control of graft rejection may exceed the problems regarding side effects. Nevertheless, it was observed that in long terms, the morbidity related to these side effects are indeed relevant. Therefore, new medicines and therapeutic schemes capable of lowering exposure to calcineurin inhibitors are being studied. There are two options of treatment established to atypical haemolytic uraemic syndrome and both of them were used in the case reports presented in this paper: plasmapheresis or plasma infusion and eculizumab, an antibody that blocks the complement system pro inflammation, pro thrombotic and lytic functions. There is great discussion regarding which one of these treatments are the most suitable for atypical haemolytic uraemic syndrome. However, the choice of the therapy depends of each patient, individually, as was seen in the cases presented in this article.

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