Open AccessVascular deposition of complement‐split products in kidney allografts with cell‐mediated rejection
Author(s) -
FEUCHT H. E.,
FELBER E.,
GOKEL M. J.,
HILLEBRAND G.,
NATTERMANN U.,
BROCKMEYER C.,
HELD E.,
RIETHMÜLLER G.,
LAND W.,
ALBERT E.
Publication year - 1991
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1991.tb02954.x
Subject(s) - complement system , immunology , antibody , peritubular capillaries , antigen , transplantation , immunoperoxidase , alternative complement pathway , biology , complement dependent cytotoxicity , complement (music) , classical complement pathway , kidney transplantation , pathology , medicine , monoclonal antibody , phenotype , antibody dependent cell mediated cytotoxicity , biochemistry , complementation , gene
SUMMARY Complement activation in 73 renal transplant biopsies was investigated by indirect immunoperoxidase staining using MoAbs reactive with complement‐split products. Intense deposition of complement fragments C4d and C3d in peritubular capillaries, indicating activation of the classical pathway, could be detected in the majority of transplanted kidneys with cell‐mediated rejections. Abundant deposition of complement‐split products was observed in 22 early biopsies from patients with high ‘immunological risk’ (i.e. previous, rejected transplants and/or circulating antibodies against HLA‐antigens). Despite negative results in the crossmatch before transplantation and paucity of immunoglobulins in transplant biopsies, antibodies directed against endothelial cell antigens should be considered as a possible cause of classical complement activation.