Allograft rejection acute

Renal allograft rejection, acute 5 mg/day for 10 to 14 days. Begin treatment once acute renal rejection is diagnosed. 

Muromonab (0KT3) Anti-CD3 Ab -Allograft rejection -Acute renal failure -Thrombotic microangiopathy 76, 78-82... 

Thymoglobulin (ATG) Anti-thymocyte globulin - Acute kidney and liver allograft rejection - Acute renal failure 110,111... 

Similar to acute lung allograft rejection, acute renal allograft rejection is also characterized by an intravascular and interstitial infiltration of mononuclear phagocytes, T cells, and occasional eosinophils. Elevated levels of RANTES/ CCL5 protein have been identified in human renal allografts undergoing acute... 

The literature on chemokines in transplantation has been extensively reviewed in recent years (7-9). In this chapter, we focus on a limited number of chemo-kine receptors where evidence for a functional role has been verified. From the plethora of chemokine receptors, this has been demonstrated for CXCR1/2 in reperfusion injury and for CCR1, CCR5, and CXCR3 during acute and chronic allograft rejection. 

Bohmig GA, Exner M, Watschinger B, Regele H. Acute humoral renal allograft rejection. Curr Opin Urol 2002 12 95-99. 

Morita K, Miura M, Paolone DR, et al. Early chemokine cascades in murine cardiac grafts regulate T cell recruitment and progression of acute allograft rejection. J Immunol 2001 167 2979-2984. 

Gao W, Topham PS, King JA, et al. Targeting of the chemokine receptor CCR1 suppresses development of acute and chronic cardiac allograft rejection. J Clin Invest 2000 105 35-44. 

Panzer U, Reinking RR, Steinmetz OM, et al. CXCR3 and CCR5 positive T-cell recruitment in acute human renal allograft rejection. Transplantation 2004 78 1341-1350. 

Hauser I A, Spiegler S, Kiss E, et al. Prediction of acute renal allograft rejection by urinary monokine induced by IFN-gamma (MIG). J Am Soc Nephrol 2005 16 1849-1858. 

Hancock WW, Gao W, Csizmadia V, Faia KL, Shemmeri N, Luster AD. Donor-derived IP-10 initiates development of acute allograft rejection. J Exp Med 2001 193 975-980. 

For short-term chnical interventions with the aim of protecting the kidney during acute reperfusion or preventing allograft rejection after transplantation, the prerequisite of parenteral administration does not constitute a serious limitation. 

Renal allograft rejection Treatment of acute allograft rejection in renal transplant patients. 

Cardiac/Hepatic allograft rejection Treatment of steroid-resistant acute allograft rejection in cardiac and hepatic transplant patients. 

Sirolimus (Rapamune) is structurally related to tacrolimus. It is approved for use as an adjunctive agent in combination with cyclosporine for prevention of acute renal allograft rejection. It blocks IL-2-dependent T-cell proliferation by inhibiting a cytoplasmic serine-threonine kinase. This mechanism of action is different from those of tacrolimus and cyclosporine. This allows sirolimus to augment the immunosuppressive effects of these drugs. 

Muromonab-(CD3) Orthoclone OKT3) is a mouse monoclonal antibody that is a purified IgG. It is used for the prevention of acute allograft rejection in kidney and hepatic transplants and as prophylaxis in cardiac transplantation. It is also used to deplete T cells in marrow from donors before bone marrow transplantation. 

B. Indications and use Orthoclone OKT3 is indicated for the treatment of acute allograft rejection in renal transplant patients and for the treatment of steroid-resistant acute allograft rejection in cardiac and hepatic transplant patients. 

H. Other considerations Daclizumab has been designated an orphan product for use in the prevention of acute renal allograft rejection. 

Indication Treatment of acute renal allograft rejection in combination with other immunosuppressants... 

Indications Prophylaxis of acute renal allograft rejection when used as part of an immunosuppressive regimen that includes steroids and cyclosporine... 

Mycophenolic acid (MPA) was isolated from cultures of Penicillium spp. in 1896 and was purified in 1913. Initially the compound was studied for its antifungal and antibacterial effects and later for its antitumor effects. Many years later, its immunosuppressive activities were recognized and after further developmental work, an ester prodrug mycophenolate mofetil was developed, which was approved by the United States Food and Drug Administration for the prevention of acute renal allograft rejection in 1995 and for heart transplant recipients in 1998. Mycophenolate mofetil is a cytotoxic agent now used for immunosuppressive therapy and is the mofetil ester of MPA, which is the active immunosuppressive agent. 

Boratynska M, Banasik M, Patrzalek D, Klinger M. 2006. Conversion from cyclosporine-based immunosuppression to tacrolimus/mycophenolate mofetil in patients with refractory and ongoing acute renal allograft rejection. Ann Transplant. 11 51-56. 

Muromonoab-CD3 is used for the treatment of acute organ transplant rejection. It is effective in preventing graft rejection after kidney, heart or liver transplantation. Muromonoab-CD3 is effective in patients who after acute cardiac or liver allograft rejection do not respond to steroid therapy. It is administered intravenously and with a dose of 5 mg/day, a general concentration range of 400-1500 ng/ml can be achieved. A serum concentration of 600-1150 ng/ml in renal transplant patients produces desirable immunosuppressive effects. The levels of CD3 expression, their production and antibodies to the drug determine its rate of clearance. In the absence of antibodies to muromonoab-CD3, its half-life is about 18 h. 

Bishop DK, Shelby J, Eichwald EJ. 1992. Mobilization of T lymphocytes following cardiac transplantation. Evidence that CD4- positive cells are required for cytotoxic T lymphocyte activation, inflammatory endothelial development, graft infiltration and acute allograft rejection. Transplantation. 53 849-857. 

Chalasani G, Li Q, Konieczny BT, Smith-Diggs L, et al. 2004. The allograft defines the type of rejection (acute vs chronic) in the face of an estabhshed effector immune response. J Immunol. 172 7813-7820. 

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