A. Kidney Tranplant Biopsy

The use of percutaneous biopsy of kidney transplant is invaluable in the prompt accurate diagnosis of parenchymal dysfunction. Often the procedure is preceded by an ultrasound to rule-out other nonparenchymal diseases as a cause of hypercreatinemia. The technique is well established and is safe. The kidney transplant biopsy can be done in the outpatient office setting. Often it is done with ultrasound guidance. Kidneys placed in the retroperitoneal iliac fossa are much more accessible to safe biopsy than those implanted in the intra-abdominal position. The site of biopsy should be the upper pole to minimize injury to the lower collecting system. Patients with prolonged bleeding time or coagulopathy should not be biopsied until these abnormalities are corrected. A 16-18 gauge biopsy needle is typically used. In most transplant programs, the renal pathologist is available to read the results of the biopsy specimen within hours of the procedure. This facilitates rapid diagnosis and institution of appropriate therapy. Most often, the biopsy is performed to confirm the clinical suspicion of acute or chronic rejection. However, occasionally, unexpected diagnoses are made such as hemolytic uremic syndrome, recurrent disease, or pyelonephritis. If changes consistent with acute nephrotoxicity of calcineurin inhibitors are observed then appropriate dosing of the immunosuppression is prescribed.

B. Rejection

1. Hyperacute Rejection

Hyperacute rejection of the renal allograft occurs when circulating preformed cytotoxic anti-donor antibodies directed to ABO blood group antigens or to donor HLA class I antigens are present. The mechanism of allograft destruction is well characterized. Antibodies bind to antigen expressed on the donor endothe-lium resulting in activation of the complement system, platelet aggregation, and microvascular obstruction. The frequency of hyperacute rejection is extremely low, being prevented by ruling-out transplant recipients with a positive pretransplant crossmatch. Hyperacute rejection may occur within minutes of revascularization of the allograft and observed intra-operatively, or it may occur hours later. Patients at risk for hyperacute rejection are those with a high past or current PRA level. There is no ability to salvage the renal allograft. Pathological examination will reveal significant interstitial hemorrhage, infiltration of neutrophils, and deposition of antibody on endothelium. A relatively new immunohis-tological technique to help determine if hyperacute rejection has occurred includes staining for complement deposition on the endothelium using an anti-c4d antibody. The ability to diagnosis hyperacute rejection histologically is often obscured because of the severe degree of kidney destruction. Other considerations would include arterial or venous thrombosis.

2. Accelerated Acute Rejection

This is a very early, rapidly progressive, and aggressive rejection reaction. It can occur within the first week of transplantation. The pathologic characteristics are massive infiltration of lymphocytes, macrophages, and plasma cells. There is injury to the renal tubules, damage of interstitial capillaries, and vascular injury of larger vessels marked by endothelial swelling. The very aggressive and rapid nature of this rejection reaction makes it difficult to reverse. Immediate therapy with anti-T-cell antibodies, in addition to pulse corticosteroids, may reverse the process. Approximately 50% of the grafts can be salvaged. It would be expected that long-term function would be compromised.

3. Acute Tubular Interstitial Cellular Rejection

This is the most common type of rejection reaction with an incidence at one year posttransplant of approximately 10 (±5)%. Typically, it occurs between 1-3 months posttransplant. It is T cell mediated and injury is directed to the renal tubules. Histopathologic examination reveals T-cell infiltration around the tubules and infiltration within the tubules, producing "tubulitis" (Fig. 6.6). The severity of rejection is defined on a continuum from mild to severe, which correlates its duration of activity.8 The gold standard for diagnosis is renal allograft biopsy. Treatment is guided by the severity of histopathological changes. Mild rejections

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