Abstract
Patients with chronic kidney disease are at significantly increased risk for cardiovascular disease and sudden cardiac death. One mechanism underlying increased cardiovascular risk in patients with renal failure includes overactivation of the sympathetic nervous system (SNS). Multiple human and animal studies have shown that central sympathetic outflow is chronically elevated in patients with both end-stage renal disease (ESRD) and chronic kidney disease (CKD). SNS overactivation, in turn, increases the risk of cardiovascular disease and sudden death by increasing arterial blood pressure, arrythmogenicity, left ventricular hypertrophy, and coronary vasoconstriction and contributes to the progression renal disease. This paper will examine the evidence for SNS overactivation in renal failure from both human and experimental studies and discuss mechanisms of SNS overactivity in CKD and therapeutic implications.
Highlights
Patients with chronic renal failure are at profoundly higher risk for cardiovascular (CV) morbidity and mortality
Patients with chronic heart failure (CHF) have elevated levels of plasma NE and muscle sympathetic nerve activity (MSNA) [22, 23], and in animal models, chronic infusion of norepinephrine caused increases in left ventricular weight [19, 24], that were independent of changes in blood pressure, implicating a causal link between sympathetic nervous system (SNS) overactivity and left ventricular hypertrophy (LVH)
Human studies using direct measurements of sympathetic nerve activity directed to muscle (MSNA) via microneurography have shown that SNS activity is chronically elevated in patients with endstage renal disease (ESRD) [13, 36, 37]
Summary
Patients with chronic renal failure are at profoundly higher risk for cardiovascular (CV) morbidity and mortality. Patients with endstage renal disease (ESRD) had a 10 to 20-fold higher risk of CV mortality [3,4,5] Such increases in CV risk are not limited to patients with the most advanced renal disease on dialysis. The pathophysiology of increased CV disease risk in CKD likely differs from that of the general population and may include factors that are specific to the diseased or ischemic kidneys. Are traditional CV risk factors such as hypertension and diabetes highly prevalent in the CKD population, but nontraditional risk factors specific to CKD and ESRD patients are highly prevalent and contribute to risk [9] These include oxidative stress, inflammation, decreased nitric oxide (NO) bioavailability, anemia, extracellular volume overload, Cardiology Research and Practice. The remainder of this paper will focus on mechanisms by which SNS overactivity increases CV risk, the evidence for SNS overactivation in renal failure, potential mechanisms of chronic sympathoexcitation in CKD (Figure 1), and therapeutic considerations
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