Mutations in CFH, CFI, C3 and THBD are associated with a worse long-term outcome than mutations in MCP.
When the defect involves genes encoding circulating proteins that are produced in the liver, such as factor H or factor I, isolated KT is not recommended, since recurrent HUS due to persisting abnormal complement factors would lead to renal graft failure.
Combined liver-kidney transplantation may represent an option in these cases?
MCP is a membrane-bound protein highly expressed in the kidney.
A dysfunction in MCP can be corrected by transplanting a normal kidney.
Surgical gene therapy.
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