Upstream, upregulation of oxidative stress related transcription factors Nrf2, p65 NF-kB and p38 MAPK led to downstream activation of an immunoregulatory response with an increase in IFN-γ content and iNOS expression, a cascade which culminated in the endpoints of accelerated renal fibrosis and atherosclerotic lesion formation within the aortic sinus in the long term. Here, NFKB1 is linked to renal fibrosis.