Renal Denervation in Moderate to Severe CKD

Abstract

Sympathetic activation contributes to the progression of CKD and is associated with adverse cardiovascular outcomes. Ablation of renal sympathetic nerves reduces sympathetic nerve activity and BP in patients with resistant hypertension and preserved renal function, but whether this approach is safe and effective in patients with an estimated GFR (eGFR) , 45 ml/min per 1.73 m 2 is unknown. We performed bilateral renal denervation in 15 patients with resistant hypertension and stage 3-4 CKD (mean eGFR, 31 ml/min per 1.73 m 2 ). We used CO 2 angiography in six patients to minimize exposure to contrast agents.Estimated GFR remained unchanged after the procedure, irrespective of the use of CO 2 angiography. Mean baseline BP 6 SD was 174622/91616 mmHg despite the use of 5.661.3 antihypertensive drugs. Mean changes in office systolic and diastolic BP at 1, 3, 6, and 12 months were 234/214, 225/211, 232/215, and 233/219 mmHg, respectively. Night-time ambulatory BP significantly decreased (P,0.05), restoring a more physiologic dipping pattern. In conclusion, this study suggests a favorable short-term safety profile and beneficial BP effects of catheter-based renal nerve ablation in patients with stage 3-4 CKD and resistant hypertension.

Renal Denervation: Unde Venis et Quo Vadis?

“…In addition to a reduction of the systolic and diastolic blood pressure (mean reduction of office blood pressure of 34/14 mmHg after 1 month, of 25/11 mmHg after 3 months, of 32/15 mmHg after 6 months and of 33/19 mmHg after 12 months), the physiological circadian rhythm with nightly blood pressure reduction was additionally restored. Renal function and retention parameters (eGFR, cystatin C, urea) as well as the renal plasma flow did not show any significant changes [64]. However, there are currently no clinical studies with larger numbers of patients proving this influence on the circadian blood pressure regulation in patients with renal insufficiency.…”

“…Studies to date have excluded patients with chronic renal diseases (GRF < 45 ml/min/1.73m 2 ) even though renal denervation seems theoretically/physiologically benefitial in these patients since limited renal function can be associated with sustained sympathetic nervous system activation [19]. This hypothesis was tested in 15 patients with chronic renal insufficiency 3°-4°(mean estimated glomerular filtration rate (eGFR) 31 ml/min/1.73 m²) with CO2 angiography being performed in 6 patients [64]. In addition to a reduction of the systolic and diastolic blood pressure (mean reduction of office blood pressure of 34/14 mmHg after 1 month, of 25/11 mmHg after 3 months, of 32/15 mmHg after 6 months and of 33/19 mmHg after 12 months), the physiological circadian rhythm with nightly blood pressure reduction was additionally restored.…”

Apparent Treatment-Resistant Hypertension and Chronic Kidney Disease: Another Cardiovascular-Renal Syndrome?

“…81 Although SYMPLICITY HTN-2 excluded patients with eGFR less than 45 mL/min/1.73 m 2 , nonrandomized, observational data suggest that renal denervation is effective and safe in patients with lower eGFR. 82,83 Bilateral renal denervation in 15 patients with Stage 3 to 4 CKD (mean eGFR 31 mL/min/1.73 m 2 ) and aTRH resulted in mean changes in office SBP and DBP at 1, 3, 6, and 12 months of 234/214, 225/211, 232/215, and 233/ 219 mm Hg, respectively. CO 2 angiography was used in 6 patients to limit contrast exposure, but no significant change in eGFR was noted with renal denervation, irrespective of the use of CO 2 angiography.…”

“…CO 2 angiography was used in 6 patients to limit contrast exposure, but no significant change in eGFR was noted with renal denervation, irrespective of the use of CO 2 angiography. 82 Importantly, despite the apparent efficacy of renal denervation for the treatment of aTRH in the SYMPLICITY HTN-2 trial and in small, proof-of concept studies in CKD, several important study design limitations affect interpretation of the results of these studies. Although randomized, patients in the medical therapy (control arm) of SYMPLICITY HTN-2 did not undergo sham procedures and, thus, placebo effect and measurement bias cannot be ruled out.…”

Renal dysfunction and increased risk of cardiotoxicity with trastuzumab therapy: a new challenge in cardio-oncology

“…Diverse mechanisms are associated with these effects, including perturbation of the renin-angiotensin system, atrial natriuretic peptide signalling and the sympathetic baroreflex system, most of which are related to hypertension. The importance of sympathetic baroreflex signaling by the kidneys in inducing cardiac stress is increasingly recognized, to the point that trials on ablation of renal sympathetic signaling in hypertensive patients are underway [7]. However, the role of RD as a risk factor for CV events in cancer therapy has to date not been entered into the cardio-oncologic equation.…”