Sympathetic Overactivity in Uremia

Abstract

Patients with chronic kidney disease frequently exhibit a sustained overactivity of the sympathetic nervous system (SNA) which is caused by neurohormonal mechanisms arising in the failing kidney. Additional potential mechanisms underlying SNA overactivity include increased levels of angiotensin II and asymmetrical dimethylarginine. Overactivity of the SNA contributes to hypertension and cardiovascular complications, and it is postulated to be a predictor of mortality in the presence of cardiovascular diseases such as asymptomatic left-ventricular dysfunction and chronic congestive heart failure. The activity of the SNA can be estimated by measurements of plasma and by spillover rates of norepinephrine (NE), microneurography (MSNA) in sympathetic muscle nerve fibers, and power spectral analysis of heart-rate and blood-pressure variability. An increase in SNA, as measured by MSNA, was found in many types of human hypertension. The pathogenesis of hypertension in renal failure is complex, and arises from the interaction of hemodynamic and neuroendocrine factors. The potential effect of erythropoietin treatment on SNA or baroreceptor activity is still unclear.