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Five years have passed since the first study on percutaneous renal denervation (RDN) to treat resistant hypertension was published.1 During its short life this technique has demonstrated its safety and efficacy in reducing blood pressure (BP), and also its appreciable indirect effects on cardiovascular remodelling and pleiotropic effects on other pathologies characterised by high sympathetic activity. Some questions about renal nerve distribution, predictors of BP response, and indices of effective denervation still remain unanswered. Moreover, the results of the Symplicity HTN-3 study are in contrast with previous findings and have raised many questions. Over time, new devices have been developed that permit a faster and more complete ablation.
Renal nerve anatomy
Sympathetic fibres to the kidneys descend the spinal cord from the brain until they reach the lower thoracic and upper lumbar spinal nerves. Fibres then pass to the adjacent ganglia in the sympathetic trunks, continuing in the postganglionic fibres which form a circumferential ‘basket-weave plexus’w1 in the adventitia of the renal artery (RA). Afferent fibres from the kidneys follow similar routes in the reverse direction.
There is still debate regarding the location and distribution of renal nerves around the RA, with some authors affirming that they are mostly distal and included in a radius of 2 mm,w2 and others demonstrating their proximal distribution with the largest nerve density between 1–4 mm around the RA (R Virmani, presented at Transcatheter Cardiovascular Therapeutics (TCT), 23 October 2012, Miami, Florida, USA) (figure 1). The latter theory is also supported by findings in animal studies.w3
Sympathetic outflow to the kidneys and other organs is regulated by the central nervous system in the nucleus tractus solitarius located in the midbrain.w4 Stimulation of α1A receptors in the renal vasculature mediates vasoconstriction and reduces renal blood flow. Adrenergic fibres are …
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