Pathologic Findings

The pathologic hallmark of large-vessel vasculitis is transmural infiltration of artery walls by mononuclear leukocytes accompanied by variable numbers of multinucleated giant cells (Fig. 9.12). This often results in

Figure 9.12. Renal artery in a nephrectomy specimen from a patient with giant cell arteritis showing (on the left) transmural inflammation with a markedly thickened intima that is impinging on the lumen (H&E).

thickening of the intima and narrowing of the lumen, which causes ischemia to the tissue supplied by the artery. Involvement of the renal artery can cause a pattern of renal artery stenosis atrophy in the renal parenchyma that is characterized by marked reduction in the size of the tubules and resultant clustering of glomeruli close to one another. This pattern of atrophy has much less interstitial fibrosis and inflammation than the isch-emic atrophy of hypertensive arterionephrosclerosis.

Large-vessel vasculitis that is causing substantial ischemic injury is treated with corticosteroids (24,25). Surgical revascularization may be required if corticosteroids are not adequate to prevent important endorgan damage.

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