Recurrence of HUS Due to CD46/MCP Mutation After Renal Transplantation: A Role for Endothelial Microchimerism

Authors

  • V. Frémeaux-Bacchi,

    1. Immunology Department, Hôpital Européen Georges Pompidou, Paris, France
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    • These authors contributed equally to this work.

  • N. Arzouk,

    1. IFRNT, Nephrology and Transplantation Department, Le Kremlin-Bicêtre Hospital, Le Kremlin-Bicêtre, Université Paris-Sud 11; France
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    • These authors contributed equally to this work.

  • S. Ferlicot,

    1. INSERM U542, Villejuif, France
    2. Anatomopathology Department, Le Kremlin-Bicêtre Hospital, Le Kremlin-Bicêtre, France
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  • B. Charpentier,

    1. IFRNT, Nephrology and Transplantation Department, Le Kremlin-Bicêtre Hospital, Le Kremlin-Bicêtre, Université Paris-Sud 11; France
    2. INSERM U542, Villejuif, France
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  • R. Snanoudj,

    1. IFRNT, Nephrology and Transplantation Department, Le Kremlin-Bicêtre Hospital, Le Kremlin-Bicêtre, Université Paris-Sud 11; France
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  • A. Dürrbach

    Corresponding author
    1. IFRNT, Nephrology and Transplantation Department, Le Kremlin-Bicêtre Hospital, Le Kremlin-Bicêtre, Université Paris-Sud 11; France
    2. INSERM U542, Villejuif, France
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* Corresponding author: Antoine Durrbach, antoine.durrbach@bct.aphp.fr

Abstract

Mutations in the gene of the membrane cofactor protein (MCP/CD46), a complement regulatory protein, were recently described as a cause of hemolytic uremic syndrome (HUS). MCP is a transmembrane glycoprotein expressed in kidneys; therefore, the transplantation of a normal kidney should not be complicated by HUS recurrence. However, we report the case of a 32-year-old woman with an MCP mutation who developed a recurrence of HUS after renal transplantation. We found that she had vascular microchimerism of endothelial cells. We suggest that recurrence may be favored by vascular microchimerism, in which the mutated protein is produced in the in the kidney graft by endothelial cells originating from recipient.

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