The genetic fingerprint of susceptibility for transplant-associated thrombotic microangiopathy

Author:

Jodele Sonata1,Zhang Kejian2,Zou Fanggeng2,Laskin Benjamin3,Dandoy Christopher E.1,Myers Kasiani C.1,Lane Adam1,Meller Jaroslav45,Medvedovic Mario5,Chen Jenny5,Davies Stella M.1

Affiliation:

1. Bone Marrow Transplantation and Immune Deficiency, and

2. Division of Human Genetics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH;

3. Division of Nephrology, The Children’s Hospital of Philadelphia, Philadelphia, PA;

4. Division of Biomedical Informatics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH; and

5. Department of Environmental Health, Division of Biostatistics and Bioinformatics, University of Cincinnati, Cincinnati, OH

Abstract

Key Points 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.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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