Acute humoral renal allograft rejection.
In kidney transplantation, it is well established that donor-specific antibodies can cause substantial graft injury. Hyperacute rejection, now virtually eliminated by routine pretransplant cytotoxic crossmatch testing, represents the prototype of humoral rejection. However, there is now increasing evidence that alloantibody-mediated immune reactions may also cause acute rejection. Acute humoral rejection, which is frequently associated with severe graft dysfunction and immunologic graft loss, represents a particular diagnostic and therapeutic challenge. Reliable detection of antibody-mediated graft injury is required to govern the application of antihumoral therapeutic strategies. This review focuses on new approaches in the diagnosis and treatment of acute humoral rejection. Special attention is given to a novel diagnostic marker, the complement split product C4d.
Böhmig
Georg A
GA
Division of Nephrology and Dialysis, Department of Medicine III, University of Vienna, Vienna, Austria. georg.boehmig@nephro.imed3.akh-wien.ac.at
Exner
Markus
M
Watschinger
Bruno
B
Regele
Heinz
H
D000917:Antibody Formation / Q000502:physiology*; D015415:Biomarkers / Q000378:metabolism; D002196:Capillaries / Q000378:metabolism; D015935:Complement C4b / Q000378:metabolism; D006084:Graft Rejection / Q000276:immunology* / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D006801:Humans; D007163:Immunosorbent Techniques; D007518:Isoantibodies / Q000032:analysis; D007674:Kidney Diseases / Q000276:immunology* / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D016030:Kidney Transplantation / Q000009:adverse effects / Q000276:immunology; D010446:Peptide Fragments / Q000378:metabolism; D010956:Plasmapheresis
D015415:Biomarkers; D007518:Isoantibodies; D010446:Peptide Fragments; D015935:Complement C4b; C032261:complement C4d