The genetic fingerprint of susceptibility for transplant-associated thrombotic microangiopathy
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- Sonata Jodele
- Bone Marrow Transplantation and Immune Deficiency, and
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- Kejian Zhang
- Division of Human Genetics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH;
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- Fanggeng Zou
- Division of Human Genetics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH;
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- Benjamin Laskin
- Division of Nephrology, The Children’s Hospital of Philadelphia, Philadelphia, PA;
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- Christopher E. Dandoy
- Bone Marrow Transplantation and Immune Deficiency, and
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- Kasiani C. Myers
- Bone Marrow Transplantation and Immune Deficiency, and
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- Adam Lane
- Bone Marrow Transplantation and Immune Deficiency, and
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- Jaroslav Meller
- Division of Biomedical Informatics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH; and
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- Mario Medvedovic
- Department of Environmental Health, Division of Biostatistics and Bioinformatics, University of Cincinnati, Cincinnati, OH
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- Jenny Chen
- Department of Environmental Health, Division of Biostatistics and Bioinformatics, University of Cincinnati, Cincinnati, OH
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- Stella M. Davies
- Bone Marrow Transplantation and Immune Deficiency, and
説明
<jats:title>Key Points</jats:title> <jats:p>HSCT recipients with multiple complement gene variants (≥3) are at high risk for severe TA-TMA. Increased numbers of complement gene variants predisposing to TMA might contribute to racial disparities in transplant-related mortality.</jats:p>
収録刊行物
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- Blood
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Blood 127 (8), 989-996, 2016-02-25
American Society of Hematology
