Office BP measurements significantly overestimate the burden of hypertension in patients with CKD and can lead to an overdiagnosis of hypertension in this population. When compared with ABPM in patients with CKD, HBPM has been shown to be superior to office measurements for the diagnosis of hypertension [35] . One week of home BP readings averaging more than 140/80 mmHg are associated with an awake ambulatory BP of more than 130/80 mmHg, which is considered “hypertensive” in the CKD population. These thresholds of SBP and DBP have been found to have both a sensitivity and specificity of more than 80 %, making HBPM useful upon which to base clinical decisions. HBPM also appears to be more accurate than office BP readings to identify CKD patients with white coat hypertension (WCH) and masked hypertension [35]. HBPM can be very useful in both diagnosis and management of hypertension in hemodialysis patients, where BP management is often difficult due to massive volume shifts [36]. Home BP readings are more reproducible from 1 week to the next when compared to pre or post-dialysis BP readings [37]. Home BP is recommended as a guide to the management of BP in dialysis patients and is useful to track changes in BP induced by reducing estimated dry-weight [37, 38]. Studies have shown that HBPM is superior when compared to pre-dialysis BP readings to manage antihypertensive therapy adjustments [39] and improves BP control [40]. The frequency and timing of HBPM in dialysis patients are important, since home BP increases on average at a rate of 4 mmHg for every 10 h of elapsed time after a recent dialysis treatment [41] . Measurement of BP soon after dialysis or just before dialysis will underestimate, or overestimate the BP, and therefore it is important to measure the BP at various intervals following dialysis [42]. It is recommended that BP be measured twice when waking up in the morning and twice before going to sleep following a midweek dialysis for 4 days [43] . These repeated midweek measurements provide an adequate number of readings to diagnose and manage hypertension. For stable dialysis patients, monthly home measurements of interdialytic BP should be encouraged. Peritoneal dialysis patients differ from hemodialysis patients in that they do not have large fluid shifts and undergo daily dialysis treatments with more stable fluid balance and BP measurements. HBPM has also been shown to be very useful in the diagnosis of hypertension in peritoneal dialysis patients [44] .

Home BP readings provide more accurate readings than office or clinic BP readings in CKD and ESRD patients when compared to an ABPM, and a number of studies have attempted to address whether HBPM correlates with target organ damage , increased CV risk, or progression of CKD .

Out-of-office BP readings in CKD patients are strongly associated with target organ damage [45] . HBPM has been shown to correlate with proteinuria and decline in eGFR [46]. Home BP measured in the morning had the strongest correlation with annual decline in eGFR [47] and as compared to office BP, HBPM is a significant predictor of decline in renal function and development of ESRD [48]. Proteinuria has been shown to be the strongest correlate of SBP by any BP measurement technique and this has been correlated more closely with both home, and ambulatory blood pressure (ABP) measurements when compared to office values [49]. In a prospective study of CKD patients, home BP readings were the most predictive of ESRD and death [50]. HBPM is useful in CKD patients to predict target organ damage , decline in renal function, CV events, and death .

In patients on hemodialysis, a U-shaped curve has been observed with SBP and mortality. Those with the lowest SBP, typically less than 100 mmHg, have the greatest mortality and there is a slight increase in mortality in patients with very high pre or post-dialysis BP readings [51]. Interdialytic BP readings done at home in dialysis patients outside the dialysis unit have been shown to predict target organ damage , including left ventricular hypertrophy (LVH) and mortality [52–57]. In an observational study using HBPM and pre and post-dialysis BP readings [12], weekly averaged BP readings were shown to have a significant correlation with left ventricular mass index and PWV, a marker of aortic stiffness, whereas pre-dialysis BP did not show a positive correlation [53]. Pulse pressures derived from within and outside the dialysis clinic, when averaged over a 1-week period have also been shown to be predictive of CV mortality and all-cause mortality [54]. In chronic hemodialysis patients, HBPM has also been shown to have a superior ability to indicate the presence of LVH when compared with pre-dialysis readings [52], and in longitudinal follow-up, patients with elevated home BP readings have higher mortality, whereas dialysis clinic BP readings do not correlate with mortality. HBPM is better correlated than office or clinic BP with target organ damage in CKD and in dialysis patients, and has greater value in predicting CV mortality and all-cause mortality. HBPM can also be incorporated into some electronic health-care records, which holds great potential to improve BP control for patients. HBPM is also attractive because it provides greater patient empowerment in their care, more insight into the connection of BP (and heart rate) with symptoms, and often better control with less medicine and greater attention to lifestyle measures by the patient. Currently, the most important deficit in the home BP initiatives is the lack of outcome data comparing home BP versus clinic BP management. This is an area of extreme need, particularly in dialysis patients. The utility of HBPM in the CKD population is shown in Table 2.2.

ABPM provides a better measure of BP control when compared to clinic or office BP measurements in the general population and in CKD . An abnormal circadian profile of BP recorded by ABPM measurements is a commonplace in CKD, and the prognostic values of ABPM for predicting renal and CV outcomes are increasingly evident.

ABPM is undertaken by wearing a device that takes BP measurements over a 24–48-h period, typically every 15–20 min during the daytime and every 30–60 min during sleep [58] . BP follows an expected circadian variation in most normotensive and most hypertensive patients, with a decline in BP during sleep. The lowest BP is often at about 3 a.m., followed by a rise during the early hours of the morning before arousal, and the highest BP tend to occur midmorning followed by a progressive fall throughout the day [59, 60]. Using 24-h ABPM, a “dipper” is generally classified as someone whose BP declines by at least 10 % or more, when comparing the average daytime with the average nighttime BP values. A blunted circadian variation of BP, termed a “non-dipper,” is defined as someone who shows less than the expected 10 % decline during the night [61]. CKD is associated with altered circadian BP rhythm, typified by a blunted amplitude of circadian variation as well as increased rates of non-dippers and even some whose BP increases during the night (“reverse dippers,” or “risers”) [62, 63]. Patients with essential hypertension have a peak BP in the early afternoon and a nocturnal BP fall of greater than 10 %; however, patients with CKD show a peak BP close to midnight and a mean nocturnal BP increase of BP. Non-dipper status is more prevalent in patients with CKD compared to patients with essential hypertension [64] and the prevalence of non-dipper status increases progressively as the renal function deteriorates reaching more than 75 % in patients with advanced (stage 5) CKD, patients on hemodialysis and peritoneal dialysis, and in renal transplant recipients [64, 65] . There is also a greater prevalence of reverse-dipper status (i.e., nighttime BP rise rather than fall) in CKD versus non-CKD patients [65]. The prevalence of reverse dippers also increases progressively from stage 1 to 5 CKD.

The use of ABPM in CKD demonstrates that approximately 50 % of patients have morning hypertension (defined as BP exceeded 135/85 mmHg during the first 2 h after awakening). The majority of these patients with morning hypertension have sustained elevation of nighttime BP (defined as BP  > 120/70 mmHg all night) resulting in a high nighttime/daytime BP ratio, suggesting that morning hypertension in CKD is of a sustained type, and not the surge type as reported in other populations [17].

ABPM is an excellent diagnostic tool to diagnose WCH and masked hypertension in CKD. WCH is present in up to about 18 % of patients with CKD leading to possible overdiagnosis and overtreatment of hypertension in CKD [66]. Conversely, masked hypertension has been shown to be present in up to 20 % of a broad range of patients with CKD [66, 67]. The African–American Study of Kidney Diseases and Hypertension (AASK), focused on one racial cohort, reported a prevalence of masked hypertension in 43 % [68]. The failure to identify masked hypertension in CKD leads to undertreatment of hypertension, and may contribute to CKD progression and CV risk. In CKD, as with general hypertensive patients who have normal kidney function, masked hypertension has been associated with the presence of LVH, the degree of proteinuria, and incident CV events [68–70].

Despite many years of availability of ABPM, there are only a few prospective studies in nondialysis CKD patients specifically investigating the prognostic significance of ABP readings for renal and CV outcomes. Data have shown that ABPM is a better tool for predicting renal and CV risk than office-based pressures in patients with various underlying causes of CKD. The predictive power for ABPM to predict renal and CV outcomes is independent of diabetes, proteinuria, level of hemoglobin, and preexisting CVD [71]. Nighttime SBP is a stronger predictor for both renal and CV end points than daytime SBP readings. Nighttime DBP is also a better predictor of fatal and nonfatal CV end points. There is also a twofold increased risk of CV end points in non-dippers and reverse dippers.

ABPM has been compared to office BP in predicting ESRD and death in patients with CKD [49]. ABPM has been shown to be a stronger predictor for ESRD and death than office BP readings and non-dipping is also associated with increased risk of total mortality and ESRD.

The longitudinal prognostic value of ABPM has also been shown using baseline ABPM data, and then assessing the rate of CKD progression and subsequent CV outcomes when evaluated over a 5-year period (70). Results showed that higher 24-h SBP, daytime, nighttime, and clinic SBP were each associated with subsequent renal and CV outcomes. However, after controlling for clinic SBP, baseline ABP readings were predictive of renal outcomes in participants with clinic SBP < 130 mmHg and of CV outcomes with no interaction based on clinic BP control.

Combining information using ABPM with eGFR in the prediction of CV outcome has been shown to be superior than using each alone over and adds prognostic value for predicting CKD and CV outcomes [72].

ABPM has also been used to adjust therapy in hypertensive children with CKD [73]. The ESCAPE trial showed that more intense BP control, defined as a mean arterial pressure below the 50th percentile as assessed using ABPM, compared with a target 24-h BP level between the 50th and the 95th percentile resulted in a substantial benefit, i.e., slowing of kidney failure progression among children with CKD. The utility of ABPM in CKD is shown in Table 2.3 .

There are several reasons why ABPM provides greater opportunity to profile CV risk and renal disease progression in patients with CKD. It provides many more readings, often more than 50 measurements, compared with a typical office visit of three readings, thereby providing a truer estimate of BP burden on the circulation and the target organs. It captures the pattern of BP over a full daily cycle and cues the provider into the success, or failure, of BP suppression during the night. In particular, ABPM accurately identifies WCH , which carries less risk than sustained hypertension, and masked hypertension, which carries more risk than normotension. By virtue of the large number of readings, it provides an opportunity to evaluate the variability of BP and heart rate, which have opposing effects on CV outcomes [74]. This information could be used to treat BP in CKD patients more accurately and identify dipping status and aid in stratification of CV risk and risk for CKD progression [75]. The CRIC study will provide more insight into the role of ABPM in CKD patients as it has more than 1500 participants studied with a focus on both CKD progression and CVD outcomes [76]. However, it is important to point out that, as with HBPM, leveraging of the superior capability of ABPM to more accurately profile a patients BP pattern and target organ damage is still largely limited to epidemiologic associations as outcome studies are lacking. This is a challenge and an opportunity for the future.

Hypertension is highly prevalent in CKD and use of traditional office or clinic BP measurements has not always correlated well with CKD progression and CV outcomes. The use of the different modalities of BP monitoring described in this chapter all have an increasingly useful role in the diagnosis and management of hypertension in CKD and in particular to aid in prediction of CKD progression and CV risk stratification. HBPM is the easiest modality to incorporate into routine management of hypertension in CKD as it is inexpensive and is associated with improved clinical care and outcomes in both nondialysis CKD patients and dialysis patients. It also directly involves patients in their care and puts some of the responsibility and ownership of improving BP control onto the patient. ABPM is the gold standard of BP measurement but, likely, will continue to be used mostly in selected patients in the clinical setting and in research studies due to the impracticalities associate with its use, including patient burden, costs, and poor reimbursement. Central BP monitoring is a promising modality as it allows arterial stiffness to be measured easily and noninvasively and it is well established that arterial stiffness is an independent predictor of CV events. Once CKD is established, the role of arterial stiffness in the progressive loss of kidney function is less clear. There is much ongoing research in this area, and in the long term, this methodology has the potential to be incorporated into routine clinical decision making when assessing CV risk as more accurate assessment of CV risk will lead to earlier interventions and potentially better outcomes in patients with CKD.