Figure 96

Features of chronic rejection. A, Arterial fibrosis and intimal thickening. B. Interstitial fibrosis and tubular atrophy. C, Typical presentation and pathologic features. Chronic rejection occurs during a span of months to years. It appears to be unresponsive to current treatment and has emerged as the major problem facing transplantation [5]. Because chronic rejection is thought to be the end result of uncontrolled repetitive acute rejection episodes or a slowly progressive inflammatory process, its onset may be as early as the first few weeks after transplantation or any time thereafter.

D, The likely sequence of events in chronic rejection and potential mediating factors for key steps. Progressive azotemia, proteinuria, and hypertension are the clinical hallmarks of chronic rejection. Immunologic and nonimmunologic mechanisms are thought to play a role in the pathogenesis of this entity. Immunologic mechanisms include antibody-mediated tissue destruction that occurs possibly secondary to antibody-dependent cellular cytotoxicity leading to obliterative arteritis, growth factors derived from macrophages and platelets leading to fibrotic degeneration, and glomerular hypertension with hyperfiltration injury due to reduced nephron mass leading to progressive glomerular sclerosis. Nonimmunologic causes can also contribute to the decline in renal function. Atheromatous renovascular disease of the transplant kidney may also be responsible for a significant number of cases of progressive graft failure.

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