Pathologic Findings

On gross examination, kidneys with AIN are enlarged with a pale cortex and a distinct corticomedullary junction. Histologically there is diffuse interstitial edema with an interstitial infiltrate of lymphocytes, monocyte-macrophages, and plasma cells to varying degrees (Fig. 13.1). Eosinophils may comprise from 0% to 10% of the infiltrate, depending on the etiology of the AIN. When there are many eosinophils, they may be focally concentrated. The inflammatory cells are often prominent at the corticome-dullary junction, and are generally confined to the cortex. Neutrophils and basophils are infrequent; large numbers of neutrophils suggest a diagnosis of acute infectious interstitial nephritis. In some cases granulomas may be found in the interstitium or around ruptured tubules. Glomeruli and vessels are usually uninvolved. The inflammation extends into the walls and lumina of tubules (tubulitis), with distal tubules more often affected than

Figure 13.1. The interstitium is edematous (tubules with normal basement membranes are separated) and infiltrated by lymphocytes, some of which are in the walls of tubules [periodic acid-schiff (PAS) stain].

proximal tubules. There are varying numbers of degenerating and regenerating tubular epithelial cells; occasionally desquamated cells may be observed in tubular lumina. Proximal tubules often have focal loss of brush border staining. Immunofluorescent studies are usually negative but infrequently reveal granular deposits of complement in the tubular basement membranes (TBMs) and rarely fibrin in the interstitium. In cases of anti-TBM antibody formation, there is linear staining of TBMs for immunoglobulin G (IgG).

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