| Literature DB >> 31970896 |
Jeremy S Nayagam1, Samuel McGrath1, Mahmoud Montasser2, Michael Delaney2, Tom D Cairns3, Kevin J Marchbank4, Harriet Denton5, Yi Yang5,6, Steven H Sacks7, H Terry Cook8, Sapna Shah9, Nigel Heaton1, Matthew C Pickering8, Abid Suddle1.
Abstract
Hereditary complement C3 deficiency is associated with recurrent bacterial infections and proliferative glomerulonephritis. We describe a case of an adult with complete deficiency of complement C3 due to homozygous mutations in C3 gene: c.1811delT (Val604Glyfs*2), recurrent bacterial infections, crescentic glomerulonephritis, and end-stage renal failure. Following isolated kidney transplantation he would remain C3 deficient with a similar, or increased, risk of infections and glomerulonephritis. As C3 is predominantly synthesized in the liver, with a small proportion of C3 monocyte derived and kidney derived, he proceeded to simultaneous liver-kidney transplantation. The procedure has been successful with restoration of his circulating C3 levels, normal liver and kidney function at 26 months of follow-up. Simultaneous liver-kidney transplant is a viable option to be considered in this rare setting.Entities:
Keywords: clinical research/practice; complement biology; immune deficiency; kidney disease: immune/inflammatory; kidney transplantation/nephrology; liver transplantation/hepatology
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Year: 2020 PMID: 31970896 DOI: 10.1111/ajt.15785
Source DB: PubMed Journal: Am J Transplant ISSN: 1600-6135 Impact factor: 9.369