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Recurrence of HUS due to CD46/MCP mutation after renal transplantation: a role for endothelial microchimerism
V Frémeaux-Bacchi1, N Arzouk, S Ferlicot
1Immunology Department, Hôpital Européen Georges Pompidou, Paris, France.
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.
Insights
Mutations in membrane cofactor protein (MCP/CD46) can cause hemolytic uremic syndrome (HUS). Even after kidney transplant, HUS recurrence is possible due to recipient-derived endothelial cells in the graft.
Area of Science:
- Nephrology
- Immunology
- Genetics
Background:
- Mutations in membrane cofactor protein (MCP/CD46), a complement regulator, are a known cause of hemolytic uremic syndrome (HUS).
- MCP is expressed in the kidneys, leading to the expectation that HUS would not recur after kidney transplantation.
Observation:
- A 32-year-old woman with an MCP mutation experienced HUS recurrence post-renal transplantation.
- Vascular microchimerism of endothelial cells was identified in the patient.
Findings:
- The patient's HUS recurred despite receiving a kidney transplant.
- The recurrence was associated with the presence of vascular microchimerism.
Implications:
- Vascular microchimerism may predispose individuals with MCP mutations to HUS recurrence after kidney transplantation.
- The mutated MCP protein might be produced in the transplanted kidney by recipient-derived endothelial cells, leading to recurrence.
