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Renal denervation—implications for chronic kidney disease

Key Points

  • Sympathetic tone and blood pressure are increased in patients with resistant hypertension and chronic kidney disease (CKD); the kidneys are a source of this increased sympathetic tone

  • Renal denervation reduces renal inflammation and injury in experimental animals and might have similar effects in patients with CKD

  • The majority of the available data suggest that renal denervation causes sustained reductions in office and ambulatory blood pressure in patients with resistant hypertension

  • No adverse effects of renal denervation on long-term renal function have been reported

  • Renal denervation seems to improve glucose metabolism and insulin sensitivity; these effects might be renoprotective in patients with CKD

Abstract

Catheter-based renal denervation to treat patients with resistant hypertension and chronic kidney disease (CKD) has generated considerable interest. Data from the majority of, but not all, observational studies and randomized controlled trials suggest that the procedure does not impair renal function and can effectively reduce office and ambulatory blood pressure in patients with primary hypertension. The putative beneficial effects of renal denervation seem to result from the interruption of renal efferent and afferent nerves. In patients with resistant hypertension and CKD, interruption of afferent reflexes might lead to a reduction in global sympathetic tone. The subsequent sustained reduction in blood pressure is expected to slow the progression of renal disease. However, renal denervation might also improve glucose metabolism, increase insulin sensitivity and reduce renal inflammation, with renoprotective effects in patients with CKD. Additional large randomized controlled trials of renal denervation in hypertensive and normotensive patients with CKD are required to precisely define the clinical value of the procedure in this population.

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Figure 1: Renal sympathetic denervation.
Figure 2: Sympathomodulation of the efferent sympathetic nervous system.
Figure 3: Effects of bilateral surgical renal denervation on albuminuria and inflammation in rats with anti-Thy1.1 nephritis.
Figure 4: Potential role of renal nerves in renal inflammation and injury.

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R.V. and R.E.S. researched the data for the article, wrote the manuscript, provided substantial contributions to discussions of the content, and reviewed and/or edited the manuscript before submission.

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Correspondence to Roland. E. Schmieder.

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R.E.S. is a member of the speakers' bureau or has received honoraria from AstraZeneca, Berlin Chemie AG, Boehringer Ingelheim, Bristol Myers Squibb, Daiichi Sankyo, Medtronic, Novartis, Servier, Takeda Pharmaceuticals and Terumo. He has acted as a consultant for AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Daiichi Sankyo, Medtronic, Novartis and Servier, and has received grant or research support (awarded to the University Hospital, University Erlangen/Nürnberg) from AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Bundesminesterium für Bildung und Forschung, Daiichi Sankyo, Novartis and Medtronic. R.V. declares that he has received grant or research support from Medtronic (awarded to the University Hospital, University Erlangen/Nürnberg).

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Veelken, R., Schmieder, R. Renal denervation—implications for chronic kidney disease. Nat Rev Nephrol 10, 305–313 (2014). https://doi.org/10.1038/nrneph.2014.59

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