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

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. 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 +/- A 2 mmHg despite an intake of 5.2 +/- A 0.1 antihypertensive drugs. Six months after renal denervation, systolic and diastolic BP decreased by 18 +/- A 2 mmHg (p < 0.0001) and 10 +/- A 1 mmHg (p < 0.001). 90 patients (65.7 %) had SBP reductions a parts per thousand yen10 mmHg (responders). After 6 months, 24-h U-Na increased by 13 % compared to baseline (236 +/- A 9 vs. 268 +/- A 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 +/- A 0.11 vs. 1.64 +/- A 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. RDN lowered BP and increased estimated U-Na and fractional sodium excretion in patients with resistant hypertension independently of renal function and antihypertensive therapy.