Rejection acute

The rejection period for a graft varies from tissue to tissue and the type of immune response involved in this process. They are divided into three types hyperacute rejection, acute rejection and chronic rejection. 

About 10 days after transplantation, acute rejection of the graft begins as a result of cell-mediated immunity. Acute rejection is a result of infiltration of large numbers of macrophages and lymphocytes into the graft. Helper T-cell activation and proliferation play a major role in this process, and both complement-dependent cell-mediated cytotoxicity and ADCC are involved in the destruction of the graft. Acute rejection could be in the form of acute vascular rejection, acute cellular rejection or both. Acute vascular rejection involves the necrosis of the blood vessel cells of the graft 

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Inhibition of immunomodulatory cytokines (Fig. 1) Anti-T-cell receptor antibodies Muromonab (OKT3, Orthoclone ) binds to the CD3 complex of the T-cell receptor and induces depletion of T-lymphocytes. It is applied to prevent acute rejection of kidney, liver, and heart allografts. Rapid side effects (within 30-60 min) include a cytokine release syndrome with fever, flu-like symptoms, and shock. Late side effects include an increased risk of viral and bacterial infections and an increased incidence of lymphproliferative diseases due to immunosuppression. 

Treatment with specific antibodies (ALG, ATG, anti-CD3, anti-CD25) is indicated during the induction phase after transplantation and in the case of acute rejection for short time periods. Therapy with nonhuman antibodies may cause sensitization. Muromonab-CD3 might initiate a cytokine release syndrome (fever, chills, headache). 

It is often difficult to differentiate ARF from acute rejection in the kidney transplant recipient, as both conditions may present with similar symptoms and physical examination findings. However, fever and graft tenderness are more likely to occur with rejection while neurotoxicity is more likely to occur with cyclosporine or tacrolimus toxicity. Kidney biopsy is often needed to confirm the diagnosis of rejection.42... 

The goal of induction therapy is to provide a high level of immunosuppression in the critical early posttransplant period when the risk of acute rejection is highest. 

Corticosteroids induce a non-specific immunosuppresion. Owing to their overwhelming incidence of adverse events, many practitioners attempt to use low-dose maintenance therapy or, in some cases, complete steroid withdrawal. Corticosteroids are also effective in reversing acute rejection. 

Acute rejection is a cell-mediated process that generally occurs within 5 to 90 days of the transplant procedure however, it can occur at any time after transplantation. This reaction is mediated through alloreactive T cells, as outlined previously. Organ-specific signs and symptoms of acute rejection are listed in Table 52-2. 

Also known as antibody-mediated rejection, humoral rejection is the process of creating graft-specific antibodies.1,4 This type of rejection occurs less frequently than cell-mediated acute rejection. Humoral rej ection is characterized by deposition of immunoglobulins and complement in allograft tissues. Treatment for this type of rejection is not well defined, yet several reports have shown that treatments such as plasmapheresis, immunoglobulin therapy, rituximab, and/or antithymocyte globulin maybe effective. 

TABLE 52-2. Organ-Specific Signs and Symptoms of an Acute Rejection Episode1 3... 

The induction agents are highly immunosuppressive and, when given prior to some organ transplants (e.g., kidney transplant), allow for significant reductions in acute rejection... 

The goals of maintenance immunosuppression are to further aid in preventing acute rejection episodes and to optimize patient and graft survival Anti-rejection medications require careful selection and dosage titration to balance the risks of rejection with the risks of adverse events. Common maintenance immunosuppressive agents can be divided into four basic medication classes ... 

Successful outcomes in solid-organ transplantation generally are measured in terms of several separate end points (1) preventing acute rejection (2) increasing 1-year graft survival ... 

Key Words Allograft transplantation chemokine receptor acute rejection chronic rejection CCR1 CCR5 CXCR3 CXCR1 CXCR2. 

Ishikawa A, Flechner SM, Goldfarb DA, et al. Quantitative assessment of the first acute rejection as a predictor of renal transplant outcome. Transplantation 1999 68 1318-1324. 

Ruster M, Sperschneider H, Funfstuck R, Stein G, Grone HJ. Differential expression of beta-chemokines MCP-1 and RANTES and their receptors CCR1, CCR2, CCR5 in acute rejection and chronic allograft nephropathy of human renal allografts. Clin Nephrol 2004 61 30-39. 

Kanmaz T, Feng P, Torrealba J, et al. Surveillance of acute rejection in baboon renal transplantation by elevation of interferon-gamma inducible protein-10 and monokine induced by interferon-gamma in urine. Transplantation 2004 78 1002-1007. 

Mange KC, Prak EL, Kamoun M, et al. Duffy antigen receptor and genetic susceptibility of African Americans to acute rejection and delayed function. Kidney Int 2004 66 1187-1192. 

Abdi R, Tran TB, Sahagun-Ruiz A, et al. Chemokine receptor polymorphism and risk of acute rejection in human renal transplantation. J Am Soc Nephrol 2002 13 754-758. 

Jamil, B. et al., Impact of acute rejection therapy on infections and malignancies in renal transplant recipients, Transplantation, 68, 1597, 1999. 

Everolimus, a derivative of sirolimus, is a novel macrocyclic immunosuppressant. Risk of acute rejection increases when the everolimus trough level falls below 3 fig/L in renal transplant patients.46... 

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