International Journal of Cardiology 190 (2015) 29–31

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Letter to the Editor

Acute effect of renal sympathetic denervation on blood pressure in refractory hypertensive patients with chronic kidney disease Márcio Galindo Kiuchi a,b, Shaojie Chen c,d, Miguel Luis Graciano a, Maria Angela Magalhães de Queiroz Carreira a, Tetsuaki Kiuchi b, Bruno Rustum Andrea e, Jocemir Ronaldo Lugon a,⁎ a

Renal Division, Department of Medicine, Universidade Federal Fluminense, Niterói, RJ, Brazil Hospital Regional Darcy Vargas, Rio Bonito, RJ, Brazil c Department of Cardiology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China d Fellowship of European Heart Rhythm Association/European Society of Cardiology, Department of Cardiology, Elisabethinen University Teaching Hospital Linz, Linz, Austria e Abteilung Elektrophysiologie, Herzzentrum, Universität Leipzig, Leipzig, Sachsen, Germany b

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Article history: Received 3 April 2015 Accepted 5 April 2015 Available online 7 April 2015 Keywords: Hypertension Chronic kidney disease Renal denervation Blood pressure reduction Improvement of renal function

The renal sympathetic denervation (RSD) led to marked reduction in systolic and diastolic blood pressure (BP) in patients with refractory hypertension and chronic kidney disease (CKD). Systemic and local autonomic nervous system disturbance plays a pivotal role in the pathogenesis of refractory hypertension and chronic kidney disease (CKD). Studies employing transcatheter renal sympathetic denervation (RSD) [1–4] showed a reduction in both systolic and diastolic blood pressure (BP) among refractory hypertensive patients. As we described previously [5,6], the reduction in office BP was evident from the 1st month until one year after RSD in refractory hypertensive patients with CKD. A recent study in animals showed the pathology of radiofrequency-derived RSD during the time and provided important knowledge of the mechanisms resulting in sustained BP reduction, and reported that the nerve injury after radiofrequency ablation was greatest at 7 days, with maximum functional nerve damage sustained ≤ 30 days. Focal terminal nerve regeneration was observed only at the sites of ablation as early as 60 days and continued to 180 days [7]. Another recent study reported a substantial decrease in ⁎ Corresponding author at: Centro de Diálise, Hospital Universitário Antônio Pedro, Rua Marquês do Paraná 303, 2°andar, Niterói, RJ 24033-900, Brazil. E-mail address: [email protected] (J.R. Lugon).

http://dx.doi.org/10.1016/j.ijcard.2015.04.039 0167-5273/© 2015 Published by Elsevier Ireland Ltd.

office systolic BP in relation to the number of ablation points at 6 months [8]. All patients in this study provided written informed consent and were selected according to previously published protocol [5]. The Committee of Ethics in Research of the Medical School of Universidade Federal Fluminense approved the study. In the period from June 2011 to December 2012, thirty consecutive patients underwent RSD. All of them had resistant hypertension and CKD (stages 2, 3 and 4), as shown in Table 1. They underwent laboratory tests and assessment of renal function at baseline and 24 h post procedure, before discharge. The procedures were performed in the catheterization laboratory with direct visualization using fluoroscopy and radiopaque contrast. In some cases, we also used three-dimensional mapping system EnSite Velocity (St. Jude Medical, St. Paul, Minnesota, USA) for construction of renal arteries and aorta anatomy, as well as for radiofrequency application in the selected sites. All patients remained under unconscious sedation. All the patients received i.v. sodium bicarbonate (3 mL/kg) and 0.9% saline for 1 h, as prophylaxis for attenuation of iodinated contrast media-associated nephrotoxicity [9,10]. The ablation procedure of the renal arteries using a standard irrigation cardiac ablation catheter was performed as previously described [5]. At the end of procedure, patients were submitted to another infusion of sodium bicarbonate (1 mL/kg/h) for 6 h [9,10]. Patients were discharged after 24 hour hospitalization, clinically stable, walking without difficulty. Bruising or aneurismal formation was not seen at the puncture site. According to the protocol [5], in the follow-up period, doppler ultrasound of the renal arteries was performed one and 6 months after the procedure in all patients and did not show any complication or change in blood flow. All the patients submitted to RSD showed highly significant reduction in office BP, both systolic and diastolic at all time points after the procedure. Accordingly, BP diminished from 185 ± 18/107 ± 13 to 140 ± 20/86 ± 12, 138 ± 15/88 ± 10, 138 ± 13/89 ± 10, 139 ± 14/ 91 ± 9, 137 ± 14/89 ± 8, 132 ± 15/86 ± 9, and 131 ± 14/87 ± 9 mm Hg at days 1 and 7, and months 1, 3, 6, and 12, post procedure, respectively (P b 0.0001 for systolic and diastolic values at every instance vs. baseline), as shown in Fig. 1. A significant correlation was found

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Table 1 General features of patients at baseline. 30 55 ± 10a 17 (57%) 21 (70%) 30.8 ± 4.9 5 (17%) 2 (7%) 6 (20%) 11 (37%) 19 (63%) 3 (10%) 4.6 ± 1.4 61.9 ± 23.9

Office Systolic BP (mmHg)

N Age (years) Female sex (%) Ethnicity (non-white) (%) Body mass index, kg/m2 Coronary artery disease (%) Atrial fibrilation (%) Stroke (%) Type 2 diabetes (%) LDL-cholesterol .130 mg/dL (%) Smoking (%) Number of antihypertensives (%) eGFR, mL/min/1.73 m2 (CKD-EPI) Stages of CKD 2 3 4 Blood pressure, mm Hg

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eGFR, estimated glomerular filtration rate. a Mean + SD.

Fig. 2. Correlation between Δ office systolic blood pressure and total radiofrequency (RF) applications per patient (n = 30).

between the decrease in office systolic blood pressure at one year (r = 0.391, P = 0.033) after the RSD and the total number of ablation spots, as shown in Fig. 2. This correlation was not observed 24 h after ablation (r = 0.276, P = 0.140). We also observed a significant increase in eGFR from baseline (61.9 ± 23.9 mL/min/1.73 m2) to 1st month (76.1 ± 32.5 mL/min/1.73 m2, P b 0.0001), 3rd month (77.2 ± 33.2 mL/min/ 1.73 m2, P b 0.0001), 6th month (80.3 ± 35.0 mL/min/1.73 m2, P b 0.0001), and at the 12th month (86.1 ± 35.2 mL/min/1.73 m2, P b 0.0001) of follow-up (Fig. 3A). Furthermore, the median albumin/ creatinine ratio (ACR) at the 1st month of follow-up (46.9, IQR: 19.0– 182.3 mg/g) was not significantly different from baseline (99.8, IQR: 38.0–192.1 mg/g), P = 0.4554. However, at the 3rd month, the median value of ACR (23.9, IQR: 10.9–159.8 mg/g) became significantly lower than baseline (P = 0.0181) a finding confirmed at the 6th month (ACR = 24.4, IQR: 10.7–96.3 mg/g), P = 0.0073, and it was sustained until the 12th month after RSD (ACR = 17.9, IQR: 10.0–100.6 mg/g), P = 0.0011 (Fig. 3B). In this study, we reported for the first time the acute (24 h) reduction in BP after RSD and its sustained effect during the follow-up period. Our results showed that the renal artery ablation at a wide range of applications of RF to produce RSD in patients with refractory hypertension and CKD seems to be effective.

Conflict of interest The authors report no relationships that could be construed as a conflict of interest.

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Follow-up Fig. 1. Office systolic (circles) and diastolic (squares) blood pressure (BP) measurements at baseline, at 24 h (h), 7 days (d), and months (m) 1, 3, 6 and 12, after renal sympathetic denervation. *P b 0.0001 vs. correspondent baseline values (n = 30). Values are presented as mean ± SEM.

Baseline

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Months Fig. 3. (A) Estimated glomerular filtration rate (eGFR), and (B) albumin:creatinine ratio (ACR) at baseline and months 1, 3, 6 and 12, after renal sympathetic denervation. *P b 0.0001 vs. correspondent baseline values (n = 30). (A) Values are presented as mean ± SD. (B) Values are presented as median with interquartile range.

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References [1] H. Krum, M. Schlaich, R. Whitbourn, et al., Catheter-based renal sympathetic denervation for resistant hypertension: a multicentre safety and proof-of-principle cohort study, Lancet 373 (2009) 1275–1281. [2] Symplicity HTN-1 Investigators, Catheter-based renal sympathetic denervation for resistant hypertension: durability of blood pressure reduction out to 24 months, Hypertension 57 (2011) 911–917. [3] Symplicity HTN-2 Investigators, M.D. Esler, H. Krum, et al., Renal sympathetic denervation in patients with treatment-resistant hypertension (The Symplicity HTN-2 Trial): a randomised controlled trial, Lancet 376 (2010) 1903–1909. [4] M. Voskuil, W.L. Verloop, P.J. Blankestijn, et al., Percutaneous renal denervation for the treatment of resistant essential hypertension; the first Dutch experience, Neth. Heart J. 19 (2011) 319–323. [5] M.G. Kiuchi, G.L. Maia, M.A. de Queiroz Carreira, et al., Effects of renal denervation with a standard irrigated cardiac ablation catheter on blood pressure and renal function in patients with chronic kidney disease and resistant hypertension, Eur. Heart J. 34 (2013) 2114–2121.

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[6] M.G. Kiuchi, S. Chen, B.R. Andrea, et al., Renal sympathetic denervation in patients with hypertension and chronic kidney disease: does improvement in renal function follow blood pressure control? J. Clin. Hypertens. (Greenwich) 16 (2014) 794–800. [7] K. Sakakura, S. Tunev, K. Yahagi, A.J. O'Brien, E. Ladich, F.D. Kolodgie, R.J. Melder, M. Joner, R. Virmani, Comparison of histopathologic analysis following renal sympathetic denervation over multiple time points, Circ. Cardiovasc. Interv. 8 (2) (Feb 2015)http://dx.doi.org/10.1161/CIRCINTERVENTIONS.114.001813 (pii: e001813). [8] J.R. Ghadri, R. Gaehwiler, M. Jaguszewski, I. Sudano, J. Osipova, R. SchoenenbergerBerzins, P. Erne, T.F. Lüscher, C. Templin, Impact of local vascular lesions assessed with optical coherence tomography and ablation points on blood pressure reduction after renal denervation, Swiss Med. Wkly. 145 (Feb 6 2015) w14102, http://dx.doi. org/10.4414/smw.2015.14102. eCollection 2015. [9] G.J. Merten, W.P. Burgess, R.A. Rittase, et al., Prevention of contrast-induced nephropathy with sodium bicarbonate: an evidence-based protocol, Crit. Pathw. Cardiol. 3 (2004) 138–143. [10] M.A. ten Dam, J.F. Wetzels, Toxicity of contrast media: an update, Neth. J. Med. 66 (2008) 416–422.

Acute effect of renal sympathetic denervation on blood pressure in refractory hypertensive patients with chronic kidney disease.

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