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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

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      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

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      Cause and consequences of sympathetic hyperactivity in chronic kidney disease.

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      Journal: Blood purification
      Keywords: Adrenergic alpha-Agonists, therapeutic use, Angiotensin II, metabolism, Angiotensin II Type 1 Receptor Blockers, Arginine, analogs & derivatives, Brain Stem, drug effects, Humans, Hyperkinesis, etiology, Hypertension, Renal, drug therapy, mortality, Imidazoles, Kidney Failure, Chronic, complications, physiopathology, Nitric Oxide Synthase, antagonists & inhibitors, Oxazoles, Receptor, Angiotensin, Type 1, Renal Dialysis, Sympathetic Nervous System, Sympatholytics

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          Abstract

          Patients with chronic kidney disease and patients undergoing hemodialysis treatment show a sustained overactivity of the sympathetic nervous system, which originates from signals arising in the failing kidneys and traveling via afferent renal nerves to cardiovascular centers in the brainstem. Additional important factors are increased levels of angiotensin II and asymmetrical dimethylarginine. The sympathetic overactivity contributes to hypertension and cardiovascular morbidity and mortality in that patient population. Sympathetic overactivity can be reduced by adrenergic receptor blockers, centrally acting sympathicolytic drugs such as moxonidine and rilmenidine, angiotensin-converting enzyme inhibition, and angiotensin II type 1 receptor antagonists. Daily short hemodialysis and long nocturnal hemodialysis may reduce the elevated sympathetic activity, possibly because of an increased clearance of asymmetrical dimethylarginine, an endogenous nitric oxide synthase inhibitor. Prospective trials examining the potential impact of both beta-blockers and centrally acting sympatholytic drugs on cardiovascular mortality in chronic kidney disease and hemodialysis patients are very much needed. Copyright 2006 S. Karger AG, Basel.

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          Sympathetic overactivity in patients with chronic renal failure.

          R Converse, T Jacobsen, R Toto … (1992)
          Hypertension is a frequent complication of chronic renal failure, but its causes are not fully understood. There is indirect evidence that increased activity of the sympathetic nervous system might contribute to hypertension in patients with end-stage renal disease, but sympathetic-nerve discharge has not been measured directly in patients or animals with chronic renal failure. We recorded the rate of postganglionic sympathetic-nerve discharge to the blood vessels in skeletal muscle by means of microelectrodes inserted into the peroneal nerve in 18 patients with native kidneys who were undergoing long-term treatment with hemodialysis (of whom 14 had hypertension), 5 patients receiving hemodialysis who had undergone bilateral nephrectomy (of whom 1 had hypertension), and 11 normal subjects. RESULTS. The mean (+/- SE) rate of sympathetic-nerve discharge was 2.5 times higher in the patients receiving hemodialysis who had not undergone nephrectomy than in the normal subjects (58 +/- 3 vs. 23 +/- 3 bursts per minute, P < 0.01). In contrast, the rate of sympathetic-nerve discharge was similar in the patients receiving hemodialysis who had undergone bilateral nephrectomy (21 +/- 6 bursts per minute) and the normal subjects. The rate of sympathetic-nerve discharge in the patients receiving hemodialysis who had not undergone nephrectomy was also significantly higher (P < 0.01) than that in the patients with bilateral nephrectomy, and it was accompanied in the former group by higher values for vascular resistance in the calf (45 +/- 4 vs. 22 +/- 4 units, P < 0.05) and mean arterial pressure (106 +/- 4 vs. 76 +/- 14 mm Hg, P < 0.05). The rate of sympathetic-nerve discharge was not correlated with either plasma norepinephrine concentrations or plasma renin activity. Chronic renal failure may be accompanied by reversible sympathetic activation, which appears to be mediated by an afferent signal arising in the failing kidneys.
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            Plasma norepinephrine predicts survival and incident cardiovascular events in patients with end-stage renal disease.

            Alessandro Cataliotti, Sebastiano Cutrupi, Francesco Rapisarda … (2002)
            Sympathetic tone is consistently raised in patients with end-stage renal disease (ESRD). We therefore tested the hypothesis that sympathetic activation is associated with mortality and cardiovascular events in a cohort of 228 patients undergoing chronic hemodialysis who did not have congestive heart failure at baseline and who had left ventricular ejection fraction >35%. The plasma concentration of norepinephrine (NE) was used as a measure of sympathetic activity. Plasma NE exceeded the upper limit of the normal range (cutoff 3.54 nmol/L) in 102 dialysis patients (45%). In a multivariate Cox regression model that included all univariate predictors of death as well as the use of sympathicoplegic agents and beta-blockers, plasma NE proved to be an independent predictor of this outcome (hazard ratio [1-nmol/L increase in plasma NE]: 1.07, 95% CI 1.01 to 1.14, P=0.03). Similarly, plasma NE emerged as an independent predictor of fatal and nonfatal cardiovascular events (hazard ratio [1-nmol/L increase in plasma NE] 1.08, 95% CI 1.02 to 1.15, P=0.01) in a model that included previous cardiovascular events, pulse pressure, age, diabetes, smoking, and use of sympathicoplegic agents and beta-blockers. The adjusted relative risk for cardiovascular complications in patients with plasma NE >75th percentile was 1.92 (95% CI 1.20 to 3.07) times higher than in those below this threshold (P=0.006). Sympathetic nerve overactivity is associated with mortality and cardiovascular outcomes in ESRD. Controlled trials with antiadrenergic drugs are needed to determine whether interference with the sympathetic system could reduce the high cardiovascular morbidity and mortality in dialysis patients.
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              Adverse mortality effect of central sympathetic inhibition with sustained-release moxonidine in patients with heart failure (MOXCON).

              , Matthias Straub, N Sharpe … (2003)
              The association between sympathetic activation and mortality in chronic heart failure and the favorable effect of beta blocking drugs has raised the possibility of therapeutic efficacy for central sympathetic inhibition with sustained-release (SR) moxonidine, an imidazoline receptor agonist. A randomized double-blind, placebo-controlled trial was initiated in 425 centers in 17 countries with a plan to enter 4533 patients with New York Heart Association class II-IV heart failure and a reduced ejection fraction. Moxonidine SR or matching placebo was titrated to a target dose of 1.5 mg BID. The trial was powered to detect a 20% reduction in mortality, which required a total of 724 deaths. An early increase in death rate and adverse events in the moxonidine SR group led to premature termination of the trial because of safety concerns after 1934 patients were entered. Final analysis revealed 54 deaths (5.5%) in the moxonidine SR group and 32 deaths (3.4%) in the placebo group during the active treatment phase. Survival curves revealed a significantly (P=0.012) worse outcome in the moxonidine SR group. Hospitalization for heart failure, acute myocardial infarction and adverse events were also more frequent in the moxonidine SR group. Plasma norepinephrine was significantly decreased by moxonidine SR (-18.8% from baseline) vs. placebo (+6.9%). Early termination of the trial limited conclusions regarding the long-term effects of central sympathetic inhibition. Nonetheless, the excess early mortality and morbidity suggest the likelihood of an adverse effect of moxonidine SR and raise concerns regarding the efficacy of generalized sympathetic inhibition in heart failure.
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                Author and article information

                Journal
                PubMed ID:: 16361848
                DOI:: 10.1159/000089444

                ScienceOpen disciplines: Chemistry
                Keywords: Adrenergic alpha-Agonists,therapeutic use,Angiotensin II,metabolism,Angiotensin II Type 1 Receptor Blockers,Arginine,analogs & derivatives,Brain Stem,drug effects,Humans,Hyperkinesis,etiology,Hypertension, Renal,drug therapy,mortality,Imidazoles,Kidney Failure, Chronic,complications,physiopathology,Nitric Oxide Synthase,antagonists & inhibitors,Oxazoles,Receptor, Angiotensin, Type 1,Renal Dialysis,Sympathetic Nervous System,Sympatholytics
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                ScienceOpen disciplines: Chemistry
                Keywords: Adrenergic alpha-Agonists, therapeutic use, Angiotensin II, metabolism, Angiotensin II Type 1 Receptor Blockers, Arginine, analogs & derivatives, Brain Stem, drug effects, Humans, Hyperkinesis, etiology, Hypertension, Renal, drug therapy, mortality, Imidazoles, Kidney Failure, Chronic, complications, physiopathology, Nitric Oxide Synthase, antagonists & inhibitors, Oxazoles, Receptor, Angiotensin, Type 1, Renal Dialysis, Sympathetic Nervous System, Sympatholytics

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