BACKGROUND/AIMS: Resistant hypertension and chronic kidney disease (CKD) are interlinked via sympathetic overdrive. Baroreflex activation therapy (BAT) has been shown to chronically reduce blood pressure (BP) in patients with resistant hypertension. The effect of BAT on renal function in CKD patients with resistant hypertension has not been reported. The aim of this study was to investigate the effect of sympathetic inhibition on renal function in CKD patients. METHODS: 23 CKD patients with resistant hypertension were prospectively treated with BAT. Analyses were performed before and 6 months after the start of BAT. The renal function was analyzed by creatinine, cystatin C, glomerular filtration rate (GFR), renin, aldosterone, fractioned and 24-hour sodium excretion and analyses of urine marker proteins. The purpose of the control group was to investigate the influence of treating patients in a center for hypertension and regression to the mean on investigated variables. RESULTS: The office mean BP decreased from 116.9 ± 20.9 mm Hg to 104.2 ± 22.2 mm Hg (p < 0.01), while the number of prescribed antihypertensive classes decreased from 6.6 ± 1.6 to 6.1 ± 1.7 (p = 0.02). Proteinuria and albuminuria decreased from a median of 283.9 and 47.7 to 136.5 (p = 0.01) and 45.0 mg/g creatinine (p = 0.01) with pronounced effects in higher CKD stage III + IV compared to I + II (p < 0.01). CKD-EPI cystatin C equation improved from 53.6 ± 22.7 to 60.4 ± 26.1 ml/min (p = 0.02). While creatinine and GFR were impaired after a period of 6 months, no changes of proteinuria, albuminuria, or BP were obtained in control patients. CONCLUSION: The data of this prospective trial demonstrate potential nephroprotective effects of BAT in therapy-resistant hypertension in CKD patients by a reduction of BP, proteinuria and moreover, a stabilization of estimated GFR.
BACKGROUND/AIMS: Resistant hypertension and chronic kidney disease (CKD) are interlinked via sympathetic overdrive. Baroreflex activation therapy (BAT) has been shown to chronically reduce blood pressure (BP) in patients with resistant hypertension. The effect of BAT on renal function in CKDpatients with resistant hypertension has not been reported. The aim of this study was to investigate the effect of sympathetic inhibition on renal function in CKDpatients. METHODS: 23 CKDpatients with resistant hypertension were prospectively treated with BAT. Analyses were performed before and 6 months after the start of BAT. The renal function was analyzed by creatinine, cystatin C, glomerular filtration rate (GFR), renin, aldosterone, fractioned and 24-hour sodium excretion and analyses of urine marker proteins. The purpose of the control group was to investigate the influence of treating patients in a center for hypertension and regression to the mean on investigated variables. RESULTS: The office mean BP decreased from 116.9 ± 20.9 mm Hg to 104.2 ± 22.2 mm Hg (p < 0.01), while the number of prescribed antihypertensive classes decreased from 6.6 ± 1.6 to 6.1 ± 1.7 (p = 0.02). Proteinuria and albuminuria decreased from a median of 283.9 and 47.7 to 136.5 (p = 0.01) and 45.0 mg/g creatinine (p = 0.01) with pronounced effects in higher CKD stage III + IV compared to I + II (p < 0.01). CKD-EPI cystatin C equation improved from 53.6 ± 22.7 to 60.4 ± 26.1 ml/min (p = 0.02). While creatinine and GFR were impaired after a period of 6 months, no changes of proteinuria, albuminuria, or BP were obtained in control patients. CONCLUSION: The data of this prospective trial demonstrate potential nephroprotective effects of BAT in therapy-resistant hypertension in CKDpatients by a reduction of BP, proteinuria and moreover, a stabilization of estimated GFR.
Authors: Mark Lipphardt; Michael J Koziolek; Luca-Yves Lehnig; Ann-Kathrin Schäfer; Gerhard A Müller; Stephan Lüders; Manuel Wallbach Journal: Clin Res Cardiol Date: 2019-04-06 Impact factor: 5.460
Authors: M Koziolek; J Beige; M Wallbach; D Zenker; G Henning; M Halbach; N Mader; F Mahfoud; G Schlieper; V Schwenger; M Hausberg; J Börgel; M Lodde; M van der Giet; J Müller-Ehmsen; J Passauer; S Parmentier; S Lüders; B K Krämer; S Büttner; F Limbourg; J Jordan; O Vonend; H-G Predel; H Reuter Journal: Internist (Berl) Date: 2017-10 Impact factor: 0.743
Authors: Manuel Wallbach; Ellen Born; Deborah Kämpfer; Stephan Lüders; Gerhard A Müller; Rolf Wachter; Michael J Koziolek Journal: Clin Res Cardiol Date: 2019-08-06 Impact factor: 5.460