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 fourfold higher in patients with AR. Administration of Met-regulated on activation, normal T cell expressed and secreted (RANTES), a chemokine receptor antagonist, suppresses recruitment of inflammatory cells into rat renal allografts. In chronic allograft nephropathy (CAN), renal lesions are induced by repeated inflammation by Th1 and/or Th2-directed antibody endothelial damage. Pro-inflammatory and pro-fibrotic mediators (IL-1, IFN-γ, tumor growth factor-β, platelet-derived growth factor, endothelin, and angiotensin II) and chemokines (RANTES) play essential roles in the development of CAN. The use of a complement regulator reduces the prevalence of CAN by minimizing I-R. Also, retinoids, which are anti-inflammatory, reduce damage consistent with CAN. In summary, there is a complex relationship between the immune system and RT organ function. Immune factors contribute to the development of organ dysfunction.