The upregulation of the oxidative stress-related transcription factors Nrf-2 and p-p65 NF-κB and the subsequent downstream phosphorylative activation of p38MAPK led to a concerted immune response characterised by increases in IFN-γ and iNOS proteins, which culminated in the endpoints of accelerated renal fibrosis and enhanced atherosclerotic lesion formation at the aortic root relative to the vehicle-treated control mice. Here, IFNG is linked to renal fibrosis.