BACKGROUND: Hypertensive chronic kidney disease (CKD) patients often have sympathetic hyperactivity. In this pilot study, we evaluated the effect of 6 weeks treatment with aliskiren on sympathetic activity in hypertensive Stages 2-4 CKD patients. METHODS: In 10 CKD patients (8 males, aged 44 ± 11 years, estimated glomerular filtration rate ( 57 ± 22 mL/min/1.73 m(2)), blood pressure and sympathetic activity [quantified by assessment of muscle sympathetic nerve activity (MSNA)] were assessed, while taken off renin-angiotensin blocker, and during the 6 weeks of treatment with aliskiren 300 mg/day. Ten other CKD patients served as control and were studied twice with an interval of 6 weeks without any change in medication, to quantify within subject reproducibility. RESULTS: In the aliskiren study group, MSNA was reduced from 36 ± 8 to 26 ± 8 bursts/min (P = 0.01). Aliskiren lowered supine systolic and diastolic blood pressure from 147 ± 10 to 120 ± 8 and from 96 ± 7 to 83 ± 7 mmHg, respectively (both P < 0.05). MSNA changed in patients treated with aliskiren [-9.6 bursts/min with 95% confidence interval (CI) -4.0 to -15.0; P-value = 0.003] but not in controls (-0.7 bursts/min with 95% CI -2.2 to 4.0; P-value = 0.6). The mean difference in change between aliskiren group and the control group was -8.9 with 95% CI of -15 to -3; P = 0.005. CONCLUSION: In hypertensive CKD patients, 6 weeks aliskiren treatment lowers blood pressure and MSNA (Clinical trial government identifier number: NCT00719316).
BACKGROUND:Hypertensive chronic kidney disease (CKD) patients often have sympathetic hyperactivity. In this pilot study, we evaluated the effect of 6 weeks treatment with aliskiren on sympathetic activity in hypertensive Stages 2-4 CKDpatients. METHODS: In 10 CKDpatients (8 males, aged 44 ± 11 years, estimated glomerular filtration rate ( 57 ± 22 mL/min/1.73 m(2)), blood pressure and sympathetic activity [quantified by assessment of muscle sympathetic nerve activity (MSNA)] were assessed, while taken off renin-angiotensin blocker, and during the 6 weeks of treatment with aliskiren 300 mg/day. Ten other CKDpatients served as control and were studied twice with an interval of 6 weeks without any change in medication, to quantify within subject reproducibility. RESULTS: In the aliskiren study group, MSNA was reduced from 36 ± 8 to 26 ± 8 bursts/min (P = 0.01). Aliskiren lowered supine systolic and diastolic blood pressure from 147 ± 10 to 120 ± 8 and from 96 ± 7 to 83 ± 7 mmHg, respectively (both P < 0.05). MSNA changed in patients treated with aliskiren [-9.6 bursts/min with 95% confidence interval (CI) -4.0 to -15.0; P-value = 0.003] but not in controls (-0.7 bursts/min with 95% CI -2.2 to 4.0; P-value = 0.6). The mean difference in change between aliskiren group and the control group was -8.9 with 95% CI of -15 to -3; P = 0.005. CONCLUSION: In hypertensiveCKDpatients, 6 weeks aliskiren treatment lowers blood pressure and MSNA (Clinical trial government identifier number: NCT00719316).
Authors: Yoshiyuki Okada; Sara S Jarvis; Stuart A Best; Tiffany B Bivens; Beverley Adams-Huet; Benjamin D Levine; Qi Fu Journal: J Physiol Date: 2013-09-23 Impact factor: 5.182
Authors: Sebastian Ewen; Christian Ukena; Dominik Linz; Roland E Schmieder; Michael Böhm; Felix Mahfoud Journal: Curr Hypertens Rep Date: 2013-08 Impact factor: 5.369