- Email: [email protected]
Response to Letter to the Editor by Drs. Yang and Yu entitled: Renal denervation in patients with chronic kidney disease
International Journal of Cardiology 235 (2017) 190
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Response to Letter to the Editor by Drs. Yang and Yu entitled: Renal denervation in patients with chronic kidney disease Dagmara Hering a, Markus P Schlaich a,b,c,⁎ a b c
School of Medicine — Royal Perth Hospital Unit, University of Western Australia, Australia Neurovascular Hypertension & Kidney Disease Laboratory, Baker Heart & Diabetes Institute, Melbourne, Australia Heart Centre Alfred Hospital, Melbourne, Australia
a r t i c l e
i n f o
Article history: Received 21 February 2017 Accepted 24 February 2017
We thank Drs. Yang and Yu for their interest in our study [1]. Sympathetic excitation is a hallmark of chronic kidney disease (CKD), evident already in early phases of renal impairment. Importantly, the magnitude of sympathetic excitation predicts mortality and CV outcomes in patients with renal disease [2]. Having previously shown that renal denervation (RDN) is safe and effective in CKD [3], we sought to investigate the trajectory of renal function both before and after RDN [1]. While improvements in relevant echocardiographic parameters have been demonstrated in CKD patients at 6 months after RDN, systematic assessment of regression of LV hypertrophy was unfortunately not performed in our study cohort. However, aside from the beneficial effects of blood pressure lowering per se, the well-established direct relationship between increased sympathetic nerve activity and hypertensive LV hypertrophy [4] suggests that RDN induced sympathetic inhibition may contribute to these effects. Indeed, we previously demonstrated a substantial and sustained reduction in sympathetic nerve firing after RDN [5]. While there appeared to be a trend towards a reduction in urinary albumin to creatinine ratio (65 ± 166 at baseline vs 57 ± 158 mg/mmol at 12 months) the changes were not statistically
⁎ Corresponding author at: School of Medicine and Pharmacology — Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, University of Western Australia, Level 3, MRF Building, Rear 50 Murray St, Perth, WA 6000, Australia. E-mail address: [email protected] (M.P. Schlaich).
http://dx.doi.org/10.1016/j.ijcard.2017.02.147 0167-5273/© 2017 Elsevier B.V. All rights reserved.
significant owing most likely to incomplete measurements, large standard deviations and relatively small sample size. The lipid profile remained essentially unchanged from baseline to 24 months followup suggesting that disruption of renal nerves does not impact significantly on cholesterol levels. Our results suggest that RDN may represent a valuable treatment option to slow or halt the progression of CKD.
Conflict of interest The authors report no relationships that could be construed as a conflict of interest.
References [1] D. Hering, P. Marusic, J. Duval, Y. Sata, G.A. Head, K.M. Denton, et al., Effect of renal denervation on kidney function in patients with chronic kidney disease, Int. J. Cardiol. 232 (2017) 93–97. [2] C. Zoccali, F. Mallamaci, S. Parlongo, S. Cutrupi, F.A. Benedetto, G. Tripepi, et al., Plasma norepinephrine predicts survival and incident cardiovascular events in patients with end-stage renal disease, Circulation 105 (2002) 1354–1359. [3] D. Hering, F. Mahfoud, A.S. Walton, H. Krum, G.W. Lambert, E.A. Lambert, et al., Renal denervation in moderate to severe CKD, J. Am. Soc. Nephrol. 23 (2012) 1250–1257. [4] M.P. Schlaich, D.M. Kaye, E. Lambert, M. Sommerville, F. Socratous, M.D. Esler, Relation between cardiac sympathetic activity and hypertensive left ventricular hypertrophy, Circulation 108 (2003) 560–565. [5] D. Hering, P. Marusic, A.S. Walton, E.A. Lambert, H. Krum, K. Narkiewicz, et al., Sustained sympathetic and blood pressure reduction 1 year after renal denervation in patients with resistant hypertension, Hypertension 64 (2014) 118–124.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Response to Letter to the Editor by Drs. Yang and Yu entitled: Renal denervation in patients with chronic kidney disease Dagmara Hering a, Markus P Schlaich a,b,c,⁎ a b c
School of Medicine — Royal Perth Hospital Unit, University of Western Australia, Australia Neurovascular Hypertension & Kidney Disease Laboratory, Baker Heart & Diabetes Institute, Melbourne, Australia Heart Centre Alfred Hospital, Melbourne, Australia
a r t i c l e
i n f o
Article history: Received 21 February 2017 Accepted 24 February 2017
We thank Drs. Yang and Yu for their interest in our study [1]. Sympathetic excitation is a hallmark of chronic kidney disease (CKD), evident already in early phases of renal impairment. Importantly, the magnitude of sympathetic excitation predicts mortality and CV outcomes in patients with renal disease [2]. Having previously shown that renal denervation (RDN) is safe and effective in CKD [3], we sought to investigate the trajectory of renal function both before and after RDN [1]. While improvements in relevant echocardiographic parameters have been demonstrated in CKD patients at 6 months after RDN, systematic assessment of regression of LV hypertrophy was unfortunately not performed in our study cohort. However, aside from the beneficial effects of blood pressure lowering per se, the well-established direct relationship between increased sympathetic nerve activity and hypertensive LV hypertrophy [4] suggests that RDN induced sympathetic inhibition may contribute to these effects. Indeed, we previously demonstrated a substantial and sustained reduction in sympathetic nerve firing after RDN [5]. While there appeared to be a trend towards a reduction in urinary albumin to creatinine ratio (65 ± 166 at baseline vs 57 ± 158 mg/mmol at 12 months) the changes were not statistically
⁎ Corresponding author at: School of Medicine and Pharmacology — Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, University of Western Australia, Level 3, MRF Building, Rear 50 Murray St, Perth, WA 6000, Australia. E-mail address: [email protected] (M.P. Schlaich).
http://dx.doi.org/10.1016/j.ijcard.2017.02.147 0167-5273/© 2017 Elsevier B.V. All rights reserved.
significant owing most likely to incomplete measurements, large standard deviations and relatively small sample size. The lipid profile remained essentially unchanged from baseline to 24 months followup suggesting that disruption of renal nerves does not impact significantly on cholesterol levels. Our results suggest that RDN may represent a valuable treatment option to slow or halt the progression of CKD.
Conflict of interest The authors report no relationships that could be construed as a conflict of interest.
References [1] D. Hering, P. Marusic, J. Duval, Y. Sata, G.A. Head, K.M. Denton, et al., Effect of renal denervation on kidney function in patients with chronic kidney disease, Int. J. Cardiol. 232 (2017) 93–97. [2] C. Zoccali, F. Mallamaci, S. Parlongo, S. Cutrupi, F.A. Benedetto, G. Tripepi, et al., Plasma norepinephrine predicts survival and incident cardiovascular events in patients with end-stage renal disease, Circulation 105 (2002) 1354–1359. [3] D. Hering, F. Mahfoud, A.S. Walton, H. Krum, G.W. Lambert, E.A. Lambert, et al., Renal denervation in moderate to severe CKD, J. Am. Soc. Nephrol. 23 (2012) 1250–1257. [4] M.P. Schlaich, D.M. Kaye, E. Lambert, M. Sommerville, F. Socratous, M.D. Esler, Relation between cardiac sympathetic activity and hypertensive left ventricular hypertrophy, Circulation 108 (2003) 560–565. [5] D. Hering, P. Marusic, A.S. Walton, E.A. Lambert, H. Krum, K. Narkiewicz, et al., Sustained sympathetic and blood pressure reduction 1 year after renal denervation in patients with resistant hypertension, Hypertension 64 (2014) 118–124.