Focal necrosis and syncytial formation within lymph nodes were identified, together with glomerulitis
and syncytial cell formation in the kidney.
(a) Transplant glomerulitis
, mild (PAS, x100), (b, c) mild infiltration of inflammatory cells including plasma cells; and mildly developed tubulitis was noted (HE, x400 (b), x200 (c)).
The identification of glomerular abnormalities, including mesangial hypercellularity or sclerosis, segmental scarring, crescent formation, glomerulitis
, or glomerular basement membrane alterations should lead to additional IF and EM studies.
Other indications of acute antibody-mediated rejection on biopsy include glomerulitis
, vasculitis, fibrin thrombi, fibrinoid necrosis, and the margination of neutrophils into the peritubular capillaries (Crespo et al., 2001).
A proportion of isolated v1 lesions maybe associated with donor specific antibodies (DSA), transplant glomerulopathy, arteriosclerosis, glomerulitis
, or C4D positivity suggesting that isolated v1 lesions in some cases may represent antibody-mediated rejection.
Serum samples from five patients experiencing renal allograft dysfunction (serum creatinine > 400 [micro]mol/L) and having biopsy-proven rejection with C4d-positive staining or notable glomerulitis
and peritubular capillaritis were analyzed (Table 1).
An urgent biopsy showed moderate glomerulitis
and the presence of inflammatory cells in peritubular capillaries, but C4d was negative.
The cardinal features observed in biopsy series included (i) light microscopy identifying a duplication of glomerular basement membrane (GBM), mesangial matrix expansion, and glomerulitis
, (ii) electron microscopy (EM) identifying a loss of endothelial fenestration, endothelial cell swelling, and mesangial matrix expansion, and (iii) immunofluorescence identifying mesangial IgM and C3 staining [+ or -] C4d in glomerular cells and peritubular capillaries [15,16].
Microcirculation inflammation, including glomerulitis
and peritubular capillaritis (PTCitis), has been recognized as a cardinal feature in the diagnosis of ABMR [9,10].
Therefore, a definitive diagnosis of rejection concurrent with viral nephropathy should only be made if there is endarteritis, fibrinoid arterial necrosis, glomerulitis
, or accumulation of the complement degradation product C4d along peritubular capillaries [29, 30].
The incidence of positive HLA-I/II antibodies (P < 0.001) and glomerulitis
(P = 0.013) is significantly higher in T-bet/ GATA3>1 group.
This inflammatory response leads to platelet aggregation and leukocyte infiltration, which eventually contribute to the pathogenesis of acute lesions such as glomerulitis
, peritubular capillaritis, microthrombi, and vessel necrosis .