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Project leader: Geoff Head (collaborative project with Markus Schlaich and Kate Denton)

Chronic kidney disease (CKD) contributes substantially to the global burden of cardiovascular (CV) morbidity and mortality. Even a moderate reduction in glomerular filtration rate (GFR) is predictive of an increased risk for coronary heart disease. Accordingly, hypertensive patients with reduced GFR are at greater risk of developing cardiovascular disease than end-stage renal disease. Unfortunately, the incidence of CKD is expected to rise further, particularly due to the increasing incidence of diabetes and hypertension. Sympathetic overactivity is implicated in the development and progression of CKD, and independently predicts cardiovascular events and mortality in end stage renal disease. Afferent signaling derived from the failing kidneys plays a causal role in renal efferent sympatho-excitation and potentiate the adverse impact of chronically increased sympathetic drive. Consequently, interruption of efferent and afferent renal fibres may provide a unique possibility to interfere with this vicious cycle not only to reduce sympathetic nervous system activation and arterial blood pressure, and to improve outcomes in this high risk patient population. While there is evidence to suggest that this technology may be particularly useful in CKD, it is essential to understand the mechanisms and potential adverse consequences of renal denervation in the setting of CKD before it can be implemented in clinical practice. We are currently determining, using a chronic rabbit model of renal failure, whether the hypotensive effects of renal denervation are due to loss of afferent or efferent nerves.

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