Autonomic dysfunction is highly prevalent in patients with chronic kidney disease (CKD). Sympathetic overactivity is commonly described (Kotanko, 2006; Grassi et al., 2012; Rubinger et al., 2013) with direct microneurograph recordings of muscle sympathetic nerve activity indicating that it is substantially elevated (Converse et al., 1992; Klein et al., 2001, 2003) and that this occurs early in the disease course (Grassi et al., 2011). Classical autonomic tests indicate that vagal outflow is also altered with impaired heart rate responses to administration of atropine, respiration, table tilt, or the Valsalva maneuver † (for review 418see Robinson and Carr, 2002). The precise underlying cause for autonomic dysfunction is unknown and likely multifactorial. With respect to sympathetic overactivity, activation of the renal afferent nerves, central and/or peripheral actions of angiotensin II, † and inhibition of brain nitric oxide synthase ‡ have been postulated as likely mechanisms (Kotanko, 2006). Notably, each of these postulated mechanisms have the capacity to impair vagal control of heart rate too (e.g., Felder, 1986; Ruggeri et al., 2000; Kawada et al., 2009). The resulting sympathetic overactivity and vagal insufficiency leads to altered sympathovagal balance at the level of heart in CKD and is a likely contributor to the increased risk of cardiac death (Herzog et al., 2008; Vaseghi and Shivkumar, 2008).
|Title of host publication||ECG time series variability analysis|
|Subtitle of host publication||engineering and medicine|
|Editors||Herbert F. Jelinek, David J. Cornforth, Ahsan H. Khandoker|
|Publisher||CRC Press, Taylor & Francis Group|
|Number of pages||21|
|Publication status||Published - 1 Jan 2017|