Inflammation and Oxidative Damage in Ischaemic Renal Disease

Ischaemic renal disease as result of atherosclerotic renovascular disease activates a complex biological response that ultimately leads to fibrosis and chronic kidney disease. Large randomised control trials have shown that renal revascularisation in patients with atherosclerotic renal artery disease does not confer any additional benefit to medical therapy alone. This is likely related to the activation of complex pathways of oxidative stress, inflammatory cytokines and fibrosis due to atherosclerotic disease and hypoxic injury due to reduced renal blood flow. New evidence from pre-clinical trials now indicates a role for specific targeted therapeutic interventions to counteract this complex pathogenesis. This evidence now suggests that the focus for those with atherosclerotic renovascular disease should be a combination of revascularisation and renoprotective therapies that target the renal tissue response to ischaemia, reduce the inflammatory infiltrate and prevent or reduce the fibrosis.

Automated summary

Ischaemic renal disease caused by atherosclerotic renovascular disease triggers a complex biological response that leads to fibrosis and chronic kidney disease. Despite large randomized control trials showing that renal revascularization does not provide additional benefits compared to medical therapy alone for patients with atherosclerotic renal artery disease, new evidence suggests targeted therapeutic interventions may be effective in countering this complex pathogenesis.