Hippokratia 2000, 4 (2): 51-65

G Vergoulas

Abstract

Renal allograft rejection is the sum of a series of immunologic events which cause graft tissue damage and graft failure. During last years, it has been shown that acute allograft rejection is caused by specific alloantigen recognition (HLA -A, -B, -DR) and non-specific inflammation caused by kidney tissue damage during transplantation. Renal allograft rejection can be discriminated into: a) hyperacute rejection that takes place minutes or hours after transplantation and is due to specific preformed anti-HLA Class I and/or anti-ABO antibodies of the recipient against the donor antigens, b) accelerated acute rejection that takes place in a few days after renal transplantation and is due to recipient presensitization against the donor antigens, c) acute rejection that happens 30% of the recipient, days or months after transplantation and d) chronic allograft nephropathy, characterized by non-reversible and inexorable fall of graft function at least three months after transplantation, accompanied by hypertension and proteinuria. This kind of rejection causes graft loss after a few months or years. The main histopathologic finding of chronic allograft nephropathy is intima hyperplasia of the vessel wall combined with glomerulosclerosis or transplant glomerulopathy and interstitial fibrosis or tubular atrophy. The factors that cause chronic allograft nephropathy are of immunologic and non-immunologic origin. Immunologic factors are acute rejection episodes, histocompatibility, previous sensitization, delayed graft function and non compliance with immunosuppressive therapy.Non-immunologic factors are the number of nephrons per kidney (donor/recipient size matching), arterial hypertension, dislipidemia and donor age.There is no hyperacute rejection therapy. Grafts with accelerated acute rejection episode have no long term survival. Corticosteroids and antilymphocyte antibodies are the drugs for antirejection therapy. In patients with chronic allograft nephropathy blood pressure control and dislipidemia therapy are necessary.

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