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Evaluation of 24-Hour Ambulatory Blood Pressure Monitoring in Patients with Chronic Kidney Disease with Normal Casual Blood Pressure.

Chronic kidney disease (CKD) is a global public health problem with high morbidity and mortality. Some patients with CKD will eventually progress to end stage renal disease (ESRD) (Amdur et al., 2016; Inaguma et al., 2017). CKD can increase the risk of and result from cardiovascular disease (CVD) (Raschenberger et al., 2015; Ricardo et al., 2015). According to the United States Renal Data System (USRDS) (2018), about 32% of individuals with CKD have hypertension, and hypertension is the second leading cause of ESRD. In one multi-center study in China of patients with CKD but who were not on dialysis, the prevalence of hypertension was 67.3%, and the control rate was 33.1%, (blood pressure [BP] less than 140/90 mmHg) (Zheng et al., 2013). Kidneys are the target organ of hypertension, as well as the initiating organ of renal hypertension, and hypertension is related to the occurrence and progression of CKD (Bloomfield et al., 2013; Zheng et al., 2013). A Japanese study showed that prehypertension is related to CKD and is one of the causes of CKD (Kanno et al., 2012). Reasonable BP control has important significance in delaying renal dysfunction, protecting kidneys, delaying ESRD, and reducing cardiovascular risks. Hypertension and CKD usually co-exist, and both are risk factors for cardiovascular events and death (Amdur et al., 2016; Bloomfield et al., 2013; Cohen, Huan, & Townsend, 2013; Zheng et al., 2013).

Ambulatory BP (ABP) can more comprehensively reflect the conditions of a patient's BP control than casual BP (CBP). CBP refers to the patient's BP as measured by physicians in a hospital, and it is sometimes referred to as the office BP. Compared with the CBP, ABP can display the circadian rhythm of BP; the existence of nocturnal hypertension, or masked hypertension (MHT); white coat hypertension; and BP load, (BPL) which can predict target-organ damage. ABP is better than CBP for reflecting the progression of CKD and end-organ damages (Cohen et al., 2013; Drawz et al., 2016; Sinha & Agarwai, 2015). Clinical reports about conditions of ABP in patients with CKD with normal CBP are few. To reveal characteristics of ABP in patients with CKD and a normal CBP, we chose a total of 350 patients with CKD (Stages 1-5) and a normal CBP for the study, aiming to provide scientific evidence for the prevention and treatment of CKD.

Materials and Methods

Subjects

A total of 350 patients with CKD (Stages 1-5) being treated in our hospital and having normal CBP were selected, among whom the majority were outpatients. The 350 patients were divided into two groups according to their CBP levels. Group 1 included patients with normal CBP (BP less than 120/80 mmHg), and Group 2 included the patients with normal CBP at high values (BP 120-139/80-89 mmHg); 50 healthy persons were selected as the Control Group. The Control Group was composed of 25 males and 25 females with normal BP (physical examination), and who were determined not to have cardiovascular and renal diseases by appropriate examinations. The mean age of individuals in the Control Group was 62.6[+ or -]11.5 years.

This study was conducted in accordance with the Declaration of Helsinki and with approval from the Ethics Committee of Fudan University. Written informed consent was obtained from all participants.

Inclusion and Exclusion Criteria

Inclusion criteria were patients with CKD (Stages 1-5) and normal CBP, free of hypertension, or who had controlled BP within normal ranges for more than a month after treatment. Exclusion criteria included CBP increasing while not receiving any antihypertensive treatments, or still exhibiting hypertension after treatment; the BP had been controlled, but the patient was now exhibiting CBP increasing on the day of ABP measurement; and having the qualification rate of ABP less than 80%, but not able to reach the standards (the qualification rate of ABP not less than 80%) when being remonitored.

Measurement of CBP

CBP was determined using a standard mercury sphygmomanometer, with the systolic blood pressure (SBP) determined at the first Korotkoff sound and the diastolic blood pressure (DBP) determined at the fifth Korotkoff sound. During the measurement, each patient was required to rest for 10 minutes, after which the BP measurement was performed at least twice (time interval of one minute) in the sitting position. Six CBP values were measured on the day of ABP measurement (once), as well as two weeks before the day of ABP measurement (twice), and were averaged and used as this patient's CBP. Each measurement was performed on the same upper arm and finished by the physician. BP less than 120/80 mmHg was defined as normal CBP, BP of 120-139/80-89 mmHg was defined as normal CBP with high value, and BP of 140/90 mmHg and above was defined as hypertension (Davis, 2015; Hernandez-Vila, 2015).

Measurement of ABP

The 24-hour ABP was monitored using one Spacelab 90207 noninvasive portable ABP monitor, with the cuff inflation pressure adjusted automatically within 40 to 259 mmHg (5.32-34.5 Kilopascal [Kpa]). The automatic adjustment was set as once every 30 minutes in the daytime and once every 60 minutes at night. The monitoring time was not less than 23 hours, and the daytime-nighttime allocation was 6:00 to 22:00 (daytime) and 22:00 to 6:00 (nighttime). Effective monitoring times within 24 hours should not be less than 80% of the counts, and each subject generally can have 32 to 40 groups of data, including SBP, DBP, BP load (BPL), and mean arterial pressure (MAP). MAP refers to the average pressure in the arteries during one cardiac cycle. Reference values of normal average ABP were 24 hours less than 130/80 mmHg, day ABP (dABP) less than 135/85 mmHg, and night ABP (nABP) less than 120/70 mmHg, MAP of 70-105 mmHg; normal BPL less than 10% (expressed as the percentage of SBP and DBP that exceeded normal ranges in a certain time); and circadian rhythm (day MAP [dMAP]-night MAP [nMAP])/dMAP) 100%. Less than 10% indicated the disappearing of the Dippers curve. The Dippers curve is also called the circadian BP rhythm. Usually, nighttime BP drops more than 10% from the daytime BP, reflecting the physiologically changing BP in 24 hours, with greater than 10% indicating the existence of the Dippers curve (Agarwal, Pappas, & Sinha, 2016; Wang, Deng, Gong, Zhang, Zhang et al., 2015; Wu et al., 2015).

Statistical Analysis

SPSS 16.0 software was used. When measurement data were normally distributed, it was expressed as mean [+ or -] standard deviation; the comparison of data among groups used the variance analysis. When measurement data were not normally distributed, it was as the median (M), 25th, 75th percentile representation (P25, P75) expressed. The comparison of data among groups used the Wilcoxon-Mann-Whitney test. Count data were expressed as frequency (n) and percentage (%), and were compared using the x2 test, with P<0.05 being considered as a statistically significant difference.

Results

General Information

Groups 1 and 2 had no statistically significant difference in age and gender composition. The average duration of disease was 85.46[+ or -]127.03 and 69.58[+ or -]89.76 months, respectively. The Control Group included 50 healthy persons who had normal BP (by physical examination) and were excluded from having cardiovascular and renal diseases by appropriate examination. Other renal diseases included gouty nephropathy, solitary kidney and renal atrophy, tumor-asso ciated nephropathy, purpura nephritis, obstructive nephropathy, aristolochic acid-related nephropathy, anodyne-induced nephropathy, and renal calculus. Detailed data in the three groups are shown in Tables 1 and 2.

Masked Hypertension and Ambulatory Blood Pressure

If setting normal CBP less than 140/90 mmHg and dAMP increasing to 135/85 mmHg or above as the diagnostic criteria of masked hypertension (MHT) (Agarwal et al., 2016), the prevalence of MHT was 19.7% (69/350). The prevalence of MHT in those without a history of hypertension was 9.7% (15/154), but in those with a history of hypertension, it was 27.6% (54/196). Among patients with CKD, it was significantly different (P<0.01). The prevalence of MHT in Group 1 was 11.0% (16/146), and in Group 2, it was 26.0% (53/204), and a significantly statistical difference (P<0.01) existed among them. Gorostidi and colleagues (2013) used 24hour ABP as the diagnostic criterion of MHT; if the above two criteria were combined and set as diagnostic criteria of MHT, the prevalence of MHT in this study would reach 25.4% (89/350). In addition to 69 cases of MHT, the remaining 281 patients with CKD exhibited simultaneous increasing of both 24-hour ABP and mean night ABP (nABP) (6.4%) in 18 cases, only 24-hour ABP increasing (0.07%, dABP and nABP were normal) in two cases, and only nABP increasing (20.6%) in 58 cases. A total of 147 patients exhibited the increasing of mean AB P, accounting for 42%. Detailed data for the three groups are shown in Tables 3 and 4.

Abnormal Blood Pressure Mode and Blood Pressure Load

The incidence of abnormal BP mode (BPM) in these patients with CKD was high (199/350, 56.9%), showing circadian rhythm disappearance (CRD), also called non-Dipperlike change. In those with normal CBP and ABP, as well as those without a history of hypertension (51 cases [472%]) showed CRD; among these patients, the incidence of abnormal BPL was 30.6% (33/108), followed by night systolic BP load (nSBPL) and night diastolic BP load (nDBPL) increasing, and day SBPL (dSBPL) and day DBPL (dDBPL) increasing. Samuels and colleagues (2012) set greater than 25% as the criterion of BPL increasing, and this study also used this criterion to determine whether BPL was increased. The time segment (24-hours, daytime, or nighttime) with the maximum BPL increasing in each patient was set as the standard to calculate the BPL increasing. Among all patients, 58.3% exhibited BPL increasing (204/350), and among these patients, 66 cases exhibited nSBPL increasing, and 68 cases exhibited nDBPL increasing (a total of 134 cases exhibited nBPL increasing, accounting for 65.7%); 49 cases exhibited dSBPL increasing, and 21 cases exhibited dDBPL increasing (a total of 70 cases exhibited dBPL increasing, accounting for 34.3%).
Box

Blood Pressure Terms and Abbreviations

Abbreviation     Term

ABP              Ambulatory blood pressure
dABP             Day ambulatory blood pressure
nABP             Night ambulatory blood pressure
ABPL             Ambulatory blood pressure load
ABPM             Ambulatory blood pressure mode
ASBPL            Ambulatory systolic blood pressure load
dASBPL           Day ambulatory systolic blood pressure load
nASBPL           Night ambulatory systolic blood pressure load
BP               Blood pressure
dBP              Day blood pressure
nBP              Night blood pressure
BPL              Blood pressure load
DBPL             Diastolic blood pressure load
SBPL             Systolic blood pressure load
dSBPL            Day systolic blood pressure load
nSBPL            Night systolic blood pressure load
dBPL             Day blood pressure load
nBPL             Night blood pressure load
BPM              Blood pressure mode
CBP              Casual blood pressure
CRD              Circadian rhythm disappearance
DBP              Diastolic blood pressure
MAP              Mean arterial pressure
dMAP             Day mean arterial pressure
nMAP             Night mean arterial pressure
SBP              Systolic blood pressure


In this study, only four cases out of the Control Group (8%) exhibited CRD and had statistically significant difference with those in Groups 1 and Group 2 (TK0.01). Detailed data in the three groups are shown in Tables 3 and 4.

Discussion

This study included a total of 350 patients with CKD in different stages and normal CBP caused by different reasons (154 cases had no history of hypertension and had normal BP at the entry, and 196 cases had history of hypertension while controlled within normal range in these patients). Results revealed:

* 147 cases with increasing ABP (42%); the mean dABP increased in 69 cases, among whom, 55 cases exhibited the simultaneous increase of dABP and nABP.

* 24-hour ABP and nABP increased in 18 cases.

* Only 24-hour ABP increased in two cases (the dABP and nABP were normal), and only nABP increased in 58 cases).

* 69 cases exhibited MHT, accounting for 19.7%. Gorostidi and colleagues (2013) used 24-hour ABP as the diagnostic criterion of MHT. If these two were combined and used as the diagnostic criteria of MHT, the prevalence of MHT in this study was 25.4% (89/350).

* 199 cases exhibited abnormal BPM (CRD) (56.9%).

* 204 cases exhibited BPL increase (58.3%), with nBPL increasing as the main form (65.7%, 134/204).

The 24-hour BP (SBP and DBP) and the mean day BP (dBP) and night BP (nBP) in Group 2 were significantly higher than those in Group 1 and the Control Group (P<0.01) (see Table 3). There was no significant difference between Group 1 and the Control Group; however, CBP in Group 1 was lower than in the Control Group, but its night ABP (nABP) (nSBP and nDBP) was significantly higher than the Control Group (P<0.01). This study found no common phenomenon that the nBPs in patients with hypertension were higher than their dBPs, which may be related to the selected patients who already controlled their BP or had no history of hypertension. Table 4 shows that 24hour BPL (SBPL and DBPL), dBPL, and nBPL in Group 2 were significantly higher than those in Group 1 and the Control Group (P<0.01). The nBPL in Group 1 was significantly higher than the Control Group (P<0.01), the dSBPL was significantly higher than the nSBPL in Group 1 and Group 2 (P<0.01), and dDBPLs were significantly lower than the nDBPLs in the same groups (P<0.01).

The rate of 24-hour ABP increased in 67 cases (32.8%), MHT increased in 53 cases (26.0%), and nABP increased in 97 cases (47.5%) in Group 2, and were significantly higher than those in Group 1, with the rate of 24-hour ABP increased in 23 cases (15.8%), MHT increased in 16 cases (11.0%), and nABP increased in 45 cases (30.8%) (P<0.01) (see Table 5). In the Control Group, 24-hour ABP did not increase, while MHT and nABP increased. The percentages of CRD were 60.3% (88 cases) and 54.4% (111 cases) in Groups 1 and 2, respectively, with no significant difference (P>0.05) between two groups. Ambulatory BPL (ABPL) increased, with 143 cases (70.1%) in Group 2, and was significantly higher than the 61 cases (41.8%) in Group 1 and the 10 cases (20.0%) in Control Group (P<0.01). The percentages of CRD and ABPL increased in Group 1 and were significantly higher than the Control Group (P<0.01).

Among 154 patients with CKD who were lacking the history of hypertension, 46 (29.9%) cases exhibited increased ABP, specifically appearing as 15 cases (9.7%) of increased dABP (also known as MHT) among these 15 patients, and 11 cases also exhibited increased nBP. Nine cases (5.8%) exhibited increased 24-hour ABP and nABP, and 22 cases (14.3%) only exhibited nBP increasing; among them, six cases exhibited increased nSBP, 13 cases exhibited increased nDBP, and three cases exhibited an increase in both. Eighty-eight cases (57.1%) exhibited abnormal BPM, and among 108 cases with both normal CBP and ABP, 51 cases (47.2%) exhibited abnormal BPM, and 33 cases (30.6%) exhibited increased BPL; 76 cases (49.4%) exhibited increased BPL, among whom 17 cases exhibited increased dBPL, and 59 cases exhibited increased nBPL. Increased nBPL accounted for the majority, especially nDBPL.

Among patients with CKD who had a history of hypertension while controlling their BP within normal range, ABP increased in 101 cases (51.5%), significantly higher than the percentage (29.9%) in patients without a history of hypertension (PK0.01). The specific manifestation included dBP increasing in 54 cases (among them, 44 cases also exhibited nBP increasing). The prevalence of MHT was 27.6%, which was significantly higher than those in Group 1 (PK0.01); nine cases (4.6%) exhibited simultaneous increasing of 24-hour ABP and nABP, two cases only exhibited 24-hour ABP increasing, and 36 cases (18.4%) only exhibited nABP increasing, showing no significant difference when compared with those in Group 1 (22 cases, 14.3%) (P>0.05). Among these patients, 19 cases exhibited nSBP and nDBP increasing, nine cases exhibited nSBP increasing, and eight cases exhibited nDBP increasing. One hundred eleven cases (56.6%) exhibited abnormal BPM, showing no significant difference than Group 1 (88 cases, 57.1%, P>0.05), indicating that a history of hypertension or not will not generate difference in the incidence of nocturnal hypertension and abnormal BPM. In 128 cases (65.3%), BPL increased, which was significantly higher than in Group 1 (76 cases (49.4%) (i<0.01). In 53 cases, dBPL increased, and 75 cases exhibited increased nBPL. The increased nBPL still accounted for the majority, but nSBPL was higher than nDBPL (50/25). Different from the finding that fewer patients in Group 1 exhibited increased nDBPL, this group mainly exhibited increased SBPL (SBPL: 79 cases; DBPL: 49 cases), and increased nBPL was higher than increased dBPL.

The prevalence of MHT in Group 1 was 11% (16/146), but in Group 2, it was 26% (53/204); there was a statistically significant difference between these two groups (i<0.01). Drawz and colleagues (2016) reported that MHT is common in patients with CKD and is related to the decrease of glomerular filtration rate, proteinuria, or cardiovascular target organ damages; thus, high attention should be paid to MHT. Table 4 reflects that normal CBP in Group 1 was lower than in the Control Group, but its nABP (SBP and DBP) was significantly higher (i<0.01). The study did not find the phenomenon of nBP being greater than dBP, which is common in hypertensive patients (Yan et al., 2015; Zhao, Fu, Ren, & Luo,2018), and it may be related to the selected patients who already controlled their BP or had no history of hypertension. It is noteworthy that 58 patients in this study only exhibited nABP increasing while normal BP in other time segments. One study (Wang, Zhang et al., 2015) named it as solitary nocturnal hypertension, which has a higher incidence in patients with CKD and is related to target organ damages. In this study, some cases were re-inspected within 3 to 12 months after the first inspection. In some cases, nBP returned to normal, while some still exhibited nocturnal hypertension. We believe patients who still have nocturnal hypertension should be given treatment. Huangfu, Duan, Xiang, and Gao (2015) reported that administering the same antihypertensive drugs to patients with primary hypertension in the morning or 2 to 4 hours before sleeping can reduce their BP. However, the latter method exhibited less incidence of BP morning peak and nocturnal hypertension, so evening was the recommended treatment time. Several studies (Kimura, 2014; Wang, Deng, Gong, Zhang, Tang et al., 2015; Wang, Zhang et al., 2015) found that nocturnal hypertension is closely related to future target organ damages and cardiovascular events, nSBP increasing is an independent risk factor for target organ damages, and more evidence proves the most sensitive predictor of cardiovascular diseases and death is nBP. Wu and colleagues (2015) found that MAP in patients with CKD Stages 45 were higher than in patients with CKD Stages 1-3, indicating MAP might be associated with risk to develop ESRD. In this study, the 24-hour MAP in Group 2 was higher than in Group 1 and in the Control Group.

In this study, the incidence of abnormal BPM (non-Dippers) was 56.9% (199/350), but the Control Group only had four cases (8%) with CRD, and there was a significant difference between them (TK0.01). Even patients with CKD who had normal CBP and ABP, and were hypertension-free still exhibited CRD (n=51, 47.2%).

This study showed that in patients with CKD regardless of hypertension, nearly half or more than half may exhibit CRD. The circadian rhythm of BP is regulated by various mechanisms, such as the autonomic nerve system, the renin-angiotensin system, and hormones. The variation with circadian rhythm of BP plays an important role to adapt the body's activities, and protects and maintains the normal vascular structure and function in the heart, brain, and kidneys. Individuals with CRD (non-Dippers) are defined as those with a nBP reduction of less than 10% of dBP. Non-Dippers may have an increased risk of cardiovascular or cerebrovascular disease (Akasaki & Ohishi, 2014). According to several researchers (Minutolo et al., 2007; Mojon et al., 2013), CRD (nonDippers) is common in patients with CKD and associated with the increased cardiovascular risks. Non-Dippers is closely related to the cardiovascular morbidity and mortality, as well as the progression of renal hypofunction, and the destruction of circadian rhythm may be associated with atherosclerosis, target organ damages, or cardiovascular events. Therefore, patients with CKD should not only control their BP well, but also change their circadian BP rhythm abnormalities. One study found the administration of antihypertensive drugs before sleeping at night can control nocturnal hypertension as well as improve the circadian rhythm of BP (Minutolo et al., 2007).

Among all patients in this study, 204 cases (58.3%) exhibited BPL increasing; 134 cases (65.7%) exhibited nBPL increasing, and the increased degrees of nSBPL and nDBPL were similar (66/68), indicating that the BPL increasing in patients with CKD who had normal CBP mainly occurred at night. Wang, Deng, Gong, Zhang, Zhang and colleagues (2015) showed that nASBPL increasing is related to the target organ damages in non-diabetic patients with CKD (left ventricular mass index, glomerular filtration rate, and proteinuria) and independent from ABP. Another study (Conkar, Yilmaz, Hacikara, Bozabali, & Mir, 2015) showed that dSBPL increasing is related to target organ damage in patients with CKD. White, Dey, and Schulman (1989) also found that 24-hour BPL is related positively to the left ventricular mass index, while negatively to the left ventricular filling pressure. It is believed that when SBPL and DBPL reach 40%, they can forecast the left ventricular functional status; when they are greater than 40%, the possibility of left ventricular hypertrophy and left ventricular diastolic dysfunction can be as high as up to 60% to 90%, especially nBPL increasing. Further, CRD can allow the heart to remain in a longterm overload status, thus causing left ventricular hypertrophy and dysfunction. BPL greater than 40% is an early warning sign of hypertensive cardiac involvement. Patients with prehypertension and hypertension can have early systolic and diastolic dysfunction, and this abnormality is related to SBPL, cardiac remodeling, or insulin resistance (Di Bello et al., 2010; Schillaci, Verdeccia, Reboldi, Pede, & Porcellati, 2000). Hypertensive patients with heart disease exhibit 24hour BPL increasing, and this can gradually lead to cardiac dysfunction (Di Bello et al., 2010; Schillaci et al., 2000). The above results suggest that BPL increasing is closely related to hypertension and hypertension-associated heart, brain, kidney, and blood vessel damages, and requires high attention.

Limitations

The sample in this study is small, especially in cases of patients with CKD Stages 4 and 5, which were less than cases of patients with CKD Stages 1 to 3. The clinical significance is for reference. The study needs to be repeated with a larger total sample and larger samples of each stage of CKD represented.

Conclusion

In summary, this study reveals significant abnormalities in patients with CKD with normal CBP (including MHT, nocturnal hypertension, BPL increasing, and CRD). Therefore, for patients with CKD, CBP cannot be used satisfactorily to evaluate whether the patient's BP has been controlled; instead, ABP should be used to comprehensively assess patients' 24-hour BP levels, especially for nBP, BPL, or the circadian rhythm of BP, which are closely related to the target organ damages, to intervene and control cardiovascular risk factors as early as possible.

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Note: Authors' biographical statements appear on the next page.

Acknowledgements: This study was supported by the Science and Technology Projects of Health Bureau of Shanghai (No 2009247).

Statement of Disclosure: The authors reported no actual or potential conflict of interest in relation to this continuing nursing education activity.

Note: The Learning Outcome, additional statements of disclosure, and instructions for CNE evaluation can be found on page 589.

Song-Yang Li, MD, is a a Chief Physician, Department of Nephrology, Jing'an District Centre Hospital of Shanghai Affiliated Fudan University (Jing'an Branch, the Affiliated Huashan Hospital of Fudan University), Shanghai, China.

Song Chen, BD, is an Attending Physician, Department of Geriatrics, Jing'an District Centre Hospital of Shanghai Affiliated Fudan University (Jing'an Branch, the Affiliated Huashan Hospital of Fudan University), Shanghai, China.

Bo Gu, MD, is a Deputy Director of the Physician, Department of Nephrology, Jing'an District Centre Hospital of Shanghai Affiliated Fudan University (Jing'an Branch, the Affiliated Huashan Hospital of Fudan University), Shanghai, China.

Jun Ma, PhD, is a Chief Physician, Department of Nephrology, Jing'an District Centre Hospital of Shanghai Affiliated Fudan University (Jing'an Branch, the Affiliated Huashan Hospital of Fudan University), Shanghai, China.

Li-Qun Wu, MD, is a Deputy Director ofthe Physician, Department of Geriatrics, Jing'an District Centre Hospital of Shanghai Affiliated Fudan University (Jing'an Branch, the Affiliated Huashan Hospital of Fudan University), Shanghai, China.

Bei-Ye Dong, MD, is an Attending Physician, Department of Nephrology, Jing'an District Centre Hospital of Shanghai Affiliated Fudan University (Jing'an Branch, the Affiliated Huashan Hospital of Fudan University), Shanghai, China.

Yin-Dan Zhao, MD, is an Attending Physician, Department of Nephrology, Jing'an District Centre Hospital of Shanghai Affiliated Fudan University (Jing'an Branch, the Affiliated Huashan Hospital of Fudan University), Shanghai, China.

Han-Qing Wang, BD, is an Attending Physician, Department of Nephrology, Jing'an District Centre Hospital of Shanghai Affiliated Fudan University (Jing'an Branch, the Affiliated Huashan Hospital of Fudan University), Shanghai, China.

Yang Yi, MD, is a Deputy Director ofthe Physician, Department of Nephrology, District Centre

Hospital of Shanghai Affiliated Fudan University (Jing'an Branch, the Affiliated Huashan Hospital of Fudan University), Shanghai, China.

Yi Xuan, MD, is an Attending Physician, Department of Nephrology, Jing'an District Centre Hospital of Shanghai Affiliated Fudan University (Jing'an Branch, the Affiliated Huashan Hospital of Fudan University), Shanghai, China.
Table 1
Clinic Data

                                              Stage of CKD n(%)
             Male/     Aging
Group        Female    (Years)                CKD1        CKD2

C (n=50)     25/25     62.6 [+ or -] 11.5
1 (n=146)    58/88     61.9 [+ or -] 14.0     47 (32.2)   46 (31.5)
2 (n=204)    78/126    63.4 [+ or -] 14.4     60 (29.4)   70 (30.3)

                                                 Duration
Group        CKD3        CKD4        CKD5        (Months)

C (n=50)
1 (n=146)    36 (24.6)   14 (9.6)    3 (2.1)     85.5 [+ or -] 127.0
2 (n=204)    55 (26.9)   14 (6.9)    5 (2.5)     69.6 [+ or -] 89.8

Table 2
Clinic Data

Grouping Primary Disease         Group 1    Group 2

Chronic pyelonephritis              34         40
IgA nephritis                       31         35
Hypertensive nephropathy            29         54
Chronic nephritis                   18         27
Chronic interstitial nephritis      10         13
Diabetic nephropathy                6          19
Ischemic nephropathy                6          0
Renal artersiosclerois              5          6
Gouty nephropathy                   3          3
Other renal disease                 4          7

Table 3
Comparison of CBP and ABP among the three groups (x [+ or -] SD)

Group                   CBP
                        SBP                         DBP

C (n=50)     122.5 [+ or -] 10.7         77.9 [+ or -] 6.0
1 (n=146)    112.0 (a) [+ or -] 8.1      72.9 (a) [+ or -] 5.6
2 (n=204)    128.9 (ab) [+ or -] 5.4     79.9 (ab) [+ or -] 6.2

Group                24-h ABPM
                     24-h SBP                    24-h DBP

C (n=50)     113.0  [+ or -] 6.7         67.8 [+ or -] 4.8
1 (n=146)    115.1 [+ or -] 12.3         68.7 [+ or -] 7.6
2 (n=204)    123.3 (ab) [+ or -] 12.0    72.0 (ab) [+ or -] 8.4

Group                Mean dBP
                       dSBP                        dDBP

C (n=50)     116.6 [+ or -] 6.9          70.8 [+ or -] 5.5
1 (n=146)    117.0 [+ or -] 12.1         70.3 [+ or -] 8.3
2 (n=204)    125.5 (ab) [+ or -] 12      73.6 (ab) [+ or -] 8.7

Group             Mean nBP (mmHg)
                       nSBP                        nDBP

C (n=50)     100.7 [+ or -] 7.1          58.8 [+ or -] 4.9
1 (n=146)    109.0 (a) [+ or -] 15.1     63.3 (a) [+ or -] 8.2
2 (n=204)    116.2 (ab) [+ or -] 15      66.3 (ab) [+ or -] 9.9

Notes: Refer to the Box on page 586 for abbreviations.

(a) P<0.01 vs. Control.

(b) P<0.01 vs. Group 1.

Table 4
Comparison of BP Load among the Three Groups M (P25, P75), %

Group           24-Hour BPL (%)
                   24-h SBPL                24-h DBPL

C (n=50)        5.1 (2.5, 12.1)           3.0 (0.0, 7.0)
1 (n=146)       5.0 (0.0, 20.5)          5.1 (0.0, 13.1)
2 (n=204)    20.6 (7.9, 38.7) (ab)    10.6 (2.6, 27.9) (ab)

Group               dBPL(%)
                     dSBPL                    dDBPL

C (n=50)        6.2 (0.0, 14.4)           3.3 (0.0, 9.0)
1 (n=146)       3.6 (0.0, 19.4)          3.4 (0.0, 10.3)
2 (n=204)    19.2 (6.3, 38.7) (ab)     7.0 (0.0, 27.6) (ab)

Group               nBPL (%)
                     nSBPL                    nDBPL

C (n=50)        0.0 (0.0, 12.5)           0.0 (0.0, 9.4)
1 (n=146)      0.0 (0.0, 18.1)ac        3.6 (0.0, 25.0)ad
2 (n=204)    18.1 (0.0, 38.1) (abc)    12.5 (0.0, 38) (abd)

Notes: Refer to the Box on page 586 for  abbreviations.

(a) P<0.01 vs. Control.

(b) P<0.01 vs. Group 1.

(c) P<0.01 dSBPL vs. nSBPL in the same group.

(d) P<0.01 dDBPL vs. nDBPL in the same group.

Table 5
Comparison of the Rate of ABP Increased, and ABPL Increased
MHT and CRD among the Three Groups

Group         24-Hour ABP            MHT         nABP Increased
                Increased
                  n (%)             n (%)             n (%)

C (n=50)          0 (0)             0 (0)             0 (0)
1 (n=146)       23 (15.8)         16 (11.0)         45 (30.8)
2 (n=204)     67 (32.8) (b)     53 (26.0) (b)     97 (47.5) (b)

Group              CRD         ABPL Increased
                               (Day or Night)
                  n (%)             n (%)

C (n=50)         4 (8.0)          10 (20.0)
1 (n=146)     88 (60.3) (a)     61 (41.8) (a)
2 (n=204)    111 (54.4) (a)    143 (70.1) (ab)

Notes: Refer to the Box on page 586 for abbreviations.

(a) P<0.01 vs Control.

(b) P<0.01 vs Group 1.
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Author:Li, Song-Yang; Chen, Song; Gu, Bo; Ma, Jun; Wu, Li-Qun; Dong, Bei-Ye; Zhao, Yin-Dan; Wang, Han-Qing;
Publication:Nephrology Nursing Journal
Article Type:Report
Date:Nov 1, 2018
Words:6083
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