Blood pressure (BP) is characterized by high variability, including changes beat-to-beat (very short term), within 24 hours (short term), from day to day (midterm), and between visits spaced by weeks, months, seasons, and even years (long term). These variations can be estimated by means of continuous beat-to-beat BP recordings, repeated conventional office BP measures, 24-hour ambulatory BP monitoring (ABPM), or home BP monitoring (HBPM) over longer time windows (Table). A main advantage of ABPM over other BP measurement techniques is represented by its ability to track BP changes occurring in daily life conditions and during 24 hours, thus allowing assessment of overall BP variability (BPV) as well as identification of its specific components, such as nocturnal hypertension and altered day-to-night BP profiles (ie, morning BP rise, nondipping pattern of BP) which become manifest early in the course of chronic kidney disease (CKD). These alterations are even more significant in subjects with end-stage renal disease (ESRD) mainly, but not exclusively, because of the marked reduction in intravascular volume immediately after hemodialysis followed by the progressive increase in volemia throughout the interdialytic period, 2 combined with an enhanced sympathetic activity. The higher frequency of alterations in 24-hour BP profiles and BPV in subjects with CKD and in those with ESRD not only makes a proper assessment and achievement of BP control more difficult in these subjects but may be prognostically relevant on the background of the evidence from longitudinal and observational studies indicating that increased BPV may predict the development of cardiovascular and renal disease, over and above the contribution of elevated mean BP levels per se 3-11 ( Figure 1). The purpose of this review is to address the currently available evidence on the role of ABPM and HBPM for the assessment and management of alterations in circadian BP profiles and in BPV in patients with CKD.
Mechanisms of BPVIn physiological conditions, BP fluctuations occurring on a beat-by-beat basis and within the 24 hours may represent a homeostatic response of neural (ie, central sympathetic drive and its reflex modulation by arterial and cardiopulmonary reflexes), humoral (catecholamines, insulin, angiotensin II, bradykinin, endothelin-1, and nitric oxide), vascular (ie, elastic properties of arteries), and rheological mechanisms (ie, blood viscosity) to environmental (weather changes), behavioral (ie, physical activity, sleep, postural changes), and emotional (ie, psychological stress) stimuli.