Figure 92

Varieties of rejection (panel A) and immune mechanisms (panel B). response, rejection of renal allografts can be commonly divided On the basis of the pathologic process and the kinetics of the rejection into hyperacute, accelerated, acute, and chronic types.

FIGURE 9-3 (See Color Plate)

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FIGURE 9-3 (See Color Plate)

Histologic features of hyperacute rejection. Hyperacute rejection is very rare and is caused by antibody-mediated damage to the graft. The clinical manifestation of hyperacute rejection is a failure of the kidney to perfuse properly on release of the vascular clamps just after vascular anastomosis is completed. The kidney initially becomes firm and then rapidly turns blue, spotted, and flabby. The presence of neutrophils in the glomeruli and peritubular capillaries in the kidney biopsy confirms the diagnosis. A, Hematoxylin and eosin stain of biopsy showing interstitial hemorrhage and extensive coagulative necrosis of tubules and glomeruli, with scattered interstitial inflammatory cells and neutrophils. B, Immunofluorescence stain of kidney with hyperacute rejection showing positive staining of fibrins.

Histologic features of acute accelerated rejection. A and B, Photomicrographs showing histologic features of acute accelerated vascular rejection. Glomerular and vascular endothelial infiltrates and swelling are visible. An accelerated rejection, which may start on the second or third day, tends to occur in the previously sensitized patient in

whom preformed anti-HLA antibodies are present. This type of rejection occurs in patients who have had a previous graft and presents with a decrease in renal function; the clinical picture is similar to that for hyperacute rejection.

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