Abstract
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.
Highlights
Reactive oxygen species are produced as part of normal cellular metabolism and as a result of environmental factors such as pollutants
atherosclerotic renovascular disease (ARVD) is often associated with atheromatous disease in other vascular systems, and patients have an increased mortality [5]; it remains an important cause of end stage kidney disease (ESKD) based on large registry data such as the USRDS data [6]
Large randomised control trials such as STAR in 2009 [8], ASTRAL in 2009 [9] and CORAL in 2014 [10] have effectively shown little overall clinical benefit following revascularisation of unselected patients with haemodynamically significant lesions (Table 1). This has led to a dramatic drop in the number of revascularisation procedures, which are reserved for complex cases such as those with acute heart failure syndromes, rapidly progressive renal impairment or hypertensive emergencies unresponsive to medical management [11]
Summary
Reactive oxygen species are produced as part of normal cellular metabolism and as a result of environmental factors such as pollutants. They are highly reactive and can damage cell structures. The kidneys are extremely metabolically active organs as they receive 25% of the total cardiac output and consume 7% of daily energy expenditure to support their various functions. They are in turn highly susceptible to oxidative damage. Previous studies have highlighted that patients with end stage kidney disease (ESKD) have much lower rates of antioxidant activity [3]
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