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Pathological study on the relationship between C4d, CD59 and C5b‐9 in acute renal allograft rejection
Author(s) -
Nishi S,
Imai N,
Ito Y,
Ueno M,
Fukase S,
Mori H,
Arakawa M,
Bassam A,
Saito K,
Takahashi K,
Gejyo F
Publication year - 2004
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/j.1399-0012.2004.00242
Subject(s) - cd59 , medicine , complement membrane attack complex , complement system , pathological , peritubular capillaries , biopsy , transplantation , immunology , immune system
In order to evaluate the activation or inhibition of the later phases of classical complement cascade in renal allograft presenting with acute rejection, particularly with C4d deposition on the peritubular capillary (PTC), we observed the expression of CD59 and C5b‐9 on the PTC. Subjective cases were divided into two groups, an acute rejection group, of 4 males and 6 females, and a normal donor group, of 5 males and 5 females. Renal biopsies were performed at the onset of acute rejection and at the transplant operation, before reperfusion. C4d deposition on PTC was found in three of 10 cases (30%) with biopsy proven acute rejection, whereas CD59 on PTC was positively expressed in all of the rejection cases. Although C5b‐9 was not observed on PTC in the acute rejection group, it was intensively deposited on the tubular basement membrane (TBM) in five cases, including the three with positive C4d on PTC. In the normal donor group, CD59 on PTC was intensively observed, whereas C5b‐9 was weakly expressed on TBM. CD59, a complement regulatory factor, works as an inhibitory factor against the formation of C5b‐9, a membrane attack complex. From our data, we noted the dissociation between the depositions of C4d and C5b‐9 on PTC. The substantially expressed CD59 on PTC may affect this dissociation between C4d and C5b‐9 on PTC. The intensive deposition of C5b‐9 on TBM in acute rejection cases may suggest an independent immunological injury attacking tubular cells.