Pathologic Findings Light Microscopy

Three forms of AHR have been recognized (Figs. 20.5 to 20.7) (19,39): (1) acute tubular injury with little inflammation, (2) peritubular and glomerular capillary inflammation with neutrophils, and (3) necrosis of arteries. Acute humoral rejection can be missed in routine sections. In one series, a component of AHR would not have been recognized in 25% of cases

Figure 20.6. Humoral rejection, type II. Neutrophils are in peritubular capillaries and glomeruli; interstitial hemorrhage is present. Anti-donor class II antibodies were demonstrable (H&E stain).
Figure 20.7. Acute humoral rejection with fibrinoid necrosis (type III). A small artery has fibrin and necrosis in the media with a scanty infiltrate (H&E stain).

without the C4d stain: 15% showed only ACR and 10% only acute tubular injury (19). The 10% acute tubular injury biopsies comprised of two donor specific antibodies (DSA+) patients with widespread C4d staining of peritubular capillaries (PTCs) that showed predominantly acute tubular injury on initial biopsy (Fig. 20.5). Later biopsies performed in one of these showed typical AHR with abundant neutrophils in PTCs and glomeruli as well as fibrinoid necrosis. Most cases have neutrophils in PTCs (Fig. 20.6). This feature is useful, but not highly sensitive or specific (19). The histologic features in the Regele et al (36) series were similarly misleading: 32% of those with C4d did not meet the Banff criteria for rejection, accounting for about 75% of the patients with AHR. In some cases arterial and arte-riolar thrombosis and glomerular thrombosis and necrosis predominate similarly to thrombotic microangiopathy (37-39). These lesions must be distinguished from the hemolytic-uremic syndrome of calcineurin inhibitor toxicity, which can also have thrombi in arterioles and glomeruli, but does not affect the peritubular capillaries (or have C4d). A minority of cases have fibrinoid necrosis, in which the arterial media shows myocyte necrosis, fragmentation of elastica, and accumulation of brightly eosino-philic material called "fibrinoid" and little mononuclear infiltrate in the intima or adventitia (Fig. 20.7). A scant infiltrate of neutrophils and eosino-phils and thrombosis may be present.

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