Inflammation after renal transplantation: Role in the development of graft dysfunction and potential therapies

Abstract

Inflammation is the response of the body to various stimuli. Mediators of inflammation include complements, pro-coagulants, cytokines, and fibrinolytics. In renal transplantation (RT), immediately after a kidney is procured, ischemia then reperfusion (I-R) occurs, involving immunologic and non-immunologic mechanisms. Inflammation causes the generation of reactive oxygen species, lipid peroxidation, and simultaneous cell necrosis and apoptosis. The mediators of I-R injury include leukocytes, platelets, and pro-coagulants. Eventually, inflammation may cause extensive tissue destruction. Attenuation of the inflammatory process is achieved by use of an interleukin (IL)-6 antibody, zinc pretreatment, and in P-selectin knockouts. The relationship between inflammation and acute rejection (AR) is present before grafting. Pre-RT serum C-reactive protein, IL-2, and interferon (IFN)-γ concentrations before, and at 1 and 2 weeks after, RT are higher in patients who develop AR. Furthermore, renal IL-6 expression is fo...