Effects of renal sympathetic denervation on urinary sodium excretion in patients with resistant hypertension

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• 作者：Janine P?ss ; Sebastian Ewen ; Roland E. Schmieder…
• 关键词：Resistant hypertension ; Renal sympathetic denervation ; 24 ; h sodium excretion ; Fractional sodium excretion ; Kawasaki formula
• 刊名：Clinical Research in Cardiology
• 出版年：2015
• 出版时间：August 2015
• 年：2015
• 卷：104
• 期：8
• 页码：672-678
• 全文大小：612 KB
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• 作者单位：Janine P?ss (1)
  Sebastian Ewen (1)
  Roland E. Schmieder (3)
  Sonja Muhler (1)
  Oliver Vonend (2)
  Christian Ott (3)
  Dominik Linz (1)
  Jürgen Geisel (4)
  Lars C. Rump (2)
  Markus Schlaich (5)
  Michael B?hm (1)
  Felix Mahfoud (1)
  
  1. Klinik für Innere Medizin III, Kardiologie, Angiologie und Internistische Intensivmedizin, Universit?tsklinikum des Saarlandes, Kirrberger Str., Geb. 40, 66421, Homburg/Saar, Germany
  3. Medizinische Klinik 4, Nephrologie und Hypertensiologie, Universit?tsklinikum Erlangen, Erlangen, Germany
  2. Klinik für Nephrologie, Universit?tsklinikum Düsseldorf, Düsseldorf, Germany
  4. Klinische Chemie und Laboratoriumsmedizin, Universit?tsklinikum des Saarlandes, Homburg/Saar, Germany
  5. Neurovascular Hypertension and Kidney Disease Laboratories, Baker IDI Heart and Diabetes Institute, Alfred Hospital, Melbourne, Australia
  
• 刊物主题：Cardiology;
• 出版者：Springer Berlin Heidelberg
• ISSN：1861-0692

文摘

Background Sympathetic overactivity increases sodium retention and contributes to the pathophysiology of hypertension. Renal sympathetic denervation lowers blood pressure and reduces sympathetic activity in certain patients with resistant hypertension. Methods and results This study aimed to assess the effect of renal denervation on urinary sodium excretion. 24-h urinary sodium excretion was estimated at baseline and after 6?months using the Kawasaki formula in 137 patients with resistant hypertension undergoing renal denervation. Sodium excretion was adjusted for cystatin C GFR and fractional sodium excretion was assessed. Mean office systolic blood pressure at baseline was 171?±?2?mmHg despite an intake of 5.2?±?0.1 antihypertensive drugs. Six months after renal denervation, systolic and diastolic BP decreased by 18?±?2?mmHg (p?<?0.0001) and 10?±?1?mmHg (p?<?0.001). 90 patients (65.7?%) had SBP reductions ?0?mmHg (responders). After 6?months, 24-h UNa increased by 13?% compared to baseline (236?±?9 vs. 268?±?9?mmol/day, p?<?0.003). This increase was most pronounced in patients with less response in BP. These findings were paralleled by a significant increase in fractional sodium excretion (1.19?±?0.11 vs. 1.64?±?0.14?%, p?<?0.0001) and were observed independently of the intake of antihypertensive drugs affecting sodium balance, such as mineralocorticoid receptor antagonists or diuretics. Conclusion RDN lowered BP and increased estimated UNa and fractional sodium excretion in patients with resistant hypertension independently of renal function and antihypertensive therapy.