Acute humoral renal transplant rejection is characterised by the following, except

Ref Robbins 8/e p 228-229; 9/e p232-233 Acute humoral rejection (rejection vasculitis) caused by antidonor antibodies also may paicipate in acute graft rejection. The histologic lesions may take the form of necro- tizing vasculitis with endothelial cell necrosis; neutrophilic infiltration; deposition of antibody, complement, and fibrin; and thrombosis. Such lesions may be associated with isch- emic necrosis of the renal parenchyma. Somewhat older subacute lesions are characterized by marked thickening of the intima by proliferating fibroblasts, myocytes, and foamy macrophages (Fig. 4-24, C). The resultant narrowing of the aerioles may cause infarction or renal coical atrophy. The proliferative vascular lesions mimic aeriosclerotic thickening and are believed to be caused by cytokines that stimulate proliferation of vascular smooth muscle cells. Local deposi- tion of complement breakdown products (specifically C4d) is used to detect antibody-mediated rejection of kidney allografts.