1.
We read with interest the eloquent opinion piece by Dr. Messerli [1] questioning the utility of a “glorified high‐tech gadget,” also known as renal denervation (RDN), as an adjunct therapeutic approach to lower blood pressure (BP) in patients with uncontrolled hypertension. Views expressed should build on the entirety of scientific evidence available—this is perhaps where the viewpoint has some shortcomings.
The critical role of renal nerves in blood pressure regulation is undoubted, as is the experimental evidence for BP lowering with RDN [2]. When we, with the late Henry Krum, performed the first two renal denervation trials out of Melbourne [3], clinical need coupled with our earlier discoveries of the neural pathophysiology of hypertension [4], not a gadget early adopter mentality, provided the motivation.
Pharmacotherapy is the mainstay of antihypertensive therapy. Professor Messerli makes special mention of amlodipine, a powerful antihypertensive drug we all use frequently in our practices, mostly in combination with other drug classes. However, as noted by the former US Surgeon General C. Everett Koop: “Drugs don't work in patients who don't take them…”. Adherence and persistence rates for amlodipine in a usual‐care setting have been reported to be 53% at 12 months [5], alternatives should be explored.
Comparing RDN with beta‐blockade is problematic. Inhibiting sympathetic outflow to a key regulatory organ such as the kidney via interference with both efferent sympathetic and afferent sensory renal nerves is fundamentally different from blocking an adrenergic receptor. A case in point is that BP response to RDN is not altered by beta‐blockade.
The magnitude of the mean BP fall with RDN is moderate and can vary substantially, perhaps a function of whether the underlying dominant pathophysiology is present or not in individual patients.
The safety profile of RDN across all studies and registries with every device available has been demonstrated to be very favorable, notwithstanding the potential risk that comes with any interventional vascular approach. Renal artery stenosis can occur naturally, and even beyond 70% stenoses treatment recommendations favor medical therapy.
Finally, the durability of BP lowering is critical. Although observational, multiple cohort studies out to ∼10 years after RDN report improved control of ambulatory systolic (12–16 mmHg) and diastolic (8–10 mmHg) on similar or less numbers of antihypertensive drugs. Histologic assessment of renal nerves after RDN demonstrate alterations of nerve integrity that make functionally relevant regrowth extremely unlikely.
No form of idolatry is helpful, growing scientific evidence is.
References
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