NDT Advance Access originally published online on April 9, 2007
Nephrology Dialysis Transplantation 2007 22(8):2217-2223; doi:10.1093/ndt/gfm164
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Prevalence and clinical correlates of white coat hypertension in chronic kidney disease
1Department of Nephrology, Second University of Naples, 2Nephrology Unit, County Hospital Solofra, 3Department of Medicine and Public Health-Research Center for Cardiovascular Disease at Second University of Naples, 4Department of Nephrology, University Federico II Naples and 5Nephrology Unit, County Hospital Nola, Italy
Correspondence and offprint requests to: Prof. Roberto Minutolo, MD, Department of Nephrology, Second University of Naples, Via Tiberio 90 I-80125, Naples, Italy. Email: roberto.minutolo{at}unina2.it
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Abstract |
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Background. The role of white coat hypertension (WCH) in the poor control of blood pressure (BP) in chronic kidney disease (CKD) is ill defined.
Methods. We measured systolic clinical (CBP) and ambulatory blood pressure (ABP) in 290 consecutive patients with non-dialysis CKD [glomerular filtration rate (GFR) <60 ml/min/1.73 m2]. We defined normotension (NOR) if CBP and daytime ABP <130 mmHg, sustained hypertension (SH) when both BP 
130 mmHg, WCH if only daytime ABP <130 mmHg, and masked hypertension (MH) when only CBP <130 mmHg.
Results. NOR patients were 15.5%, WCH 31.7%, SH 46.9% and MH 5.9%. Due to the high prevalence of WCH, achievement of BP target (<130 mmHg) was more than doubled by daytime ABP than CBP (47.2 vs 21.4%). WCH was characterized by prevalence of diabetes (31.5%), left ventricular hypertrophy (LVH; 50.0%) and CBP values (146 ± 12 mmHg) lower than in SH (41.9%, 71.3% and 158 ± 18 mmHg) but greater than in NOR (17.8%, 37.8% and 118 ± 7 mmHg). Among patients with CBP 130 mmHg, the independent risk of having SH rather than WCH increased in the presence of higher CBP [Odds ration (OR) 1.61, 95% confidence intervals (CI) 1.29–2.02], LVH (OR 1.94, 95% CI 1.03–3.63) and proteinuria (OR 3.12, 95% CI 1.31–7.43). In the WCH group, 24 h, daytime and nighttime ABP were 118 ± 7/68 ± 8, 120 ± 7/71 ± 8 and 112 ± 12/63 ± 9 mmHg, respectively.
Conclusions. In CKD, WCH is highly prevalent and can be predicted in the absence of higher CBP, LVH and proteinuria. In these patients, pursuing a low BP target may not be safe because of the risk of cardio–renal hypoperfusion especially at nighttime.
Keywords: ambulatory blood pressure monitoring; cardiovascular risk; chronic kidney disease; hypertension; white coat hypertension
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Introduction |
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Patients with chronic kidney disease (CKD) are characterized by well-defined cardiovascular (CV) risk, that is so high that exceeds that of progressing towards end-stage renal disease (ESRD) [1–3]. Among the modifiable CV risk factors, uncontrolled hypertension plays a major role, being the most common risk factor in patients with a glomerular filtration rate (GFR) <60 ml/min [4]. Indeed, optimal blood pressure (BP) control, that is, achieving a clinical BP target of <130/80 mmHg, is likely crucial to reduce CV morbidity and mortality and retard progression of renal disease [5–9]. Nevertheless, worldwide achievement of BP targets remains dramatically low even in patients steadily followed in tertiary care [4,10–12].
Several factors have been claimed to explain the unsatisfactory BP management in CKD, such as resistance to antihypertensive therapy, too low BP target and clinical inertia [9]. In particular, a possible cause of therapeutic inertia may be represented by the occurrence of white coat hypertension (WCH) also in treated patients, that is, the concomitant presence of uncontrolled clinical BP (CBP) and normal ambulatory blood pressure (ABP). This phenomenon may lead to a less intensive antihypertensive intervention when physicians take into account also ABP monitoring or home recordings rather than planning the therapeutic approach exclusively on the basis of office measurement. While white coat phenomenon has been extensively investigated in essential hypertension and in the general population, only few studies are available in CKD [13–15]. These studies, however, have been performed in a group of older-aged male veterans with mild CKD (GFR <90 ml/min) characterized by a high mortality rate. The results obtained in this selected group of patients suggest that WCH has a prevalence of 
25% [13], and that the predictive value of ABP monitoring on global outcome is greater with respect to office BP [14,15]. However, clinical characteristics of WCH patients were not reported; in particular, whether the white coat effect is characterized by a specific CV risk profile or it is a phenomenon merely dependent on the ABP variability remains undefined. This aspect becomes critical when considering that intensification of antihypertensive therapy in patients with high office BP levels, but normal BP during the rest of the day, can lead to hypotensive episodes and consequent increase of the risk of renal ischaemia and mortality [7,16–18].
We, therefore, designed the present cross-sectional study in order to assess, in unselected CKD patients with moderate-to-advanced CKD (GFR <60 ml/min), the prevalence and the clinical correlates of white coat phenomenon. This analysis was performed by using systolic BP since it is well recognized that in CKD hypertension is predominantly systolic [4,13], and that this component of BP, which is the best predictor of mortality and progression of renal disease [6,14,18,19], is the most difficult to control in Europe [4,9,11,12].
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Methods |
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This is a cross-sectional study that enrolled consecutive patients in outpatient clinics of four nephrology units (Second University of Naples, University Federico II Naples, County Hospital of Nola and County Hospital of Solofra) from 1 January 2005 to 31 December 2005. Patients were included if age was
18 years and GFR estimated by means of the abbreviated four-component MDRD equation (eGFR), was <60 ml/min/1.73 m2. Exclusion criteria were as follows: change of eGFR >30% in the previous 3 months, change of antihypertensive therapy in the 2 weeks prior to the study, atrial fibrillation, dialytic treatment or renal transplantation. Medical history, including history of CV event (coronary artery disease, congestive heart failure, cerebrovascular and peripheral vascular disease), left ventricular hypertrophy (LVH) detected at either electrocardiography or echocardiography, demographic and laboratory data, and current therapy were collected at the study visit. All patients were informed about the study protocol and gave their written informed consent before study enrolment.
Clinic blood pressure measurement
During the physician's visit (8–11 AM), CBP was measured, according to the recommendations of the European Society of Hypertension [20], in a quiet environment with a mercury sphygmomanometer with the patient in a sitting position after 5 min of rest. Systolic and diastolic BP values (Korotkoff phase I and phase V, respectively) represented in each visit the mean of three different readings measured at 5 min intervals. The reported values of CBP are the mean of the values recorded in the 2 days in which the ABP device was installed and removed. Sphygmomanometric measurements were obtained by the same physician who was not aware of the results of ABP recordings.
Ambulatory blood pressure monitoring
The patients underwent 24 h ABP monitoring by Spacelabs 90207 monitor, that has been previously validated and recommended for clinical use [21]. The cuff size was chosen on the basis of the patient's arm circumference and it was fixed to the non-dominant arm. Three blood pressure readings were taken in the morning (8–11 AM) concomitantly with sphygmomanometric measurements to ensure that the average of the two sets of values did not differ for more than 5 mmHg. The monitor recorded BP every 15 min during the period 7:00 AM to 11:00 PM and every 30 min during the period 11:00 PM to 7:00 AM. Daytime and nighttime periods were derived from the diaries recorded by the patients during the ABP monitoring. Monitoring was always done on a working day and under eventual usual antihypertensive treatment. The patients had no access to the ABP values. Monitoring was considered adequate if 14 systolic and diastolic measurements were obtained during the day and seven during the night [20].
Patient groups
The definition of patient groups was made according to the most recent trials on ABP in CKD patients [13–15]. Patients were defined truly normotensive (NOR) if both systolic CBP and systolic daytime ABP were <130 mmHg. Patients with poorly controlled hypertension in office (CBP 130 mmHg) were divided in two subgroups according to ABP: one subgroup with WCH, when systolic daytime ABP <130 mmHg and one subgroup defined as sustained hypertension (SH), when systolic daytime ABP 130 mmHg. Patients with systolic CBP <130 mmHg and systolic daytime ABP 130 mmHg were considered to have masked hypertension (MH). Dipping status was defined as night/day ratio of systolic ABP <0.90.
Statistical analysis
Data were analysed using SPSS version 12.0. (SPSS Inc., Chicago, IL, USA). Continuous variables were expressed as mean and SD, and compared with analysis of variance (ANOVA) and Bonferroni post hoc test for comparison among the four groups while Student's t-test was used to perform comparison between the two groups. Categorical variables were expressed as percentage and compared by using 
2 test.
Logistic regression analysis was used among patients with systolic CBP 130 mmHg (WCH and SH patients) to identify factors associated with a risk of having SH. For each of the 14 baseline characteristics, a univariate logistic regression model was used to estimate the odds ratio (OR) and its 95% confidence interval (CI); variables that failed to have a significant effect were eliminated before developing a multivariate model. On the contrary, age and gender were included a priori in the model because of their widely recognized effect on BP levels and in order to allow future comparisons. Model performance was assessed by means of C-index.
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Results |
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Among 331 eligible patients, 290 were enrolled (Figure 1). In these patients, valid ABP readings were obtained from 93.4% of the readings planned (i.e. 80 readings over 24 h) with no difference between daytime and nighttime. The number of measurements was 74.5 ± 4.9 during a period of monitoring of 23.1 ± 1.8 h. We classified 15.5% of patients as NOR, while 46.9% had SH. WCH was detected in 31.7% of patients. MH was detected in only 5.9% of patients. The presence of about one-third of WCH led to a significant difference in the prevalence of BP <130 mmHg according to the technique of BP measurement used. In fact, when using office measurement of BP, we found that controlled BP was achieved in 21.4% of patients (95% CI 16.7–26.1); conversely, by means of daytime ABP measurement, prevalence of BP<130 mmHg markedly raised to 47.2% (95% CI 41.5–53.0), P < 0.0001 vs CBP. Patients during the ABP monitoring did not report any symptomatic hypotensive episode.
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The description of CV risk profile in the four groups of patients is reported in Tables 1 and 2. True normotensives had younger age with respect to the other groups of patients. Prevalence of diabetes progressively increased from NOR to SH. Similarly, prevalence of LVH rose in parallel with the worsening of BP control, in the presence of unchanged haemoglobin values. A similar trend was detected for the prevalence of previous CV events. The eGFR was similar in the four groups while SH patients showed higher levels of proteinuria. Systolic CBP was lower in NOR than in MH group; similarly, in WCH patients it was significantly lower than in SH. The comparison of ABP between NOR and WCH evidenced in the latter group higher values of systolic values of 24 h, daytime and nighttime ABP; the same held true when MH was compared with sustained hypertensives. The night/day ratio, as well as the prevalence of dippers, did not differ in the four groups (Table 2).
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In WCH, the distribution of systolic BP measured as CBP, 24 h, day and night ABP is reported in Figure 2. The 5th percentile was 103.9, 104.0 and 92.7 mmHg for 24 h, daytime and nighttime systolic ABP, respectively. A systolic value below 100 mmHg was detected in four patients (4.4%) for 24 h ABP, two patients (2.2%) for daytime ABP and 13 patients (14.1%) for nighttime ABP. When considering the NOR group, the 5th percentile was 105.0 mmHg for systolic CBP and 100.3 mmHg for systolic daytime ABP; of course, a lower limit was detected for nighttime systolic ABP (87.3 mmHg) and consequently for 24 h ABP (97.2 mmHg).
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When repeating this analysis in NOR, the prevalence of patients with a systolic value below 100 mmHg was similar to that detected in WCH group (2.2%, 2.2% and 15.1% for 24 h, daytime and nighttime ABP, respectively).
We performed logistic regression to evaluate in patients with high systolic CBP the clinical, laboratory and demographic features associated with the risk of having also uncontrolled daytime systolic ABP, that is, the risk of having SH rather than WCH. In this analysis we included age, gender and those clinical and laboratory data that resulted as significant at univariate analysis (Table 3). We found that within the group of patients with office hypertension (CBP 130 mmHg), the independent factors associated to a greater risk of having also a systolic daytime ABP 130 mmHg (sustained hypertension) are LVH, proteinuria >1 g/day and higher systolic CBP. Specifically, the risk increased by 61% for each 10 mmHg of increase in CBP 130 mmHg and by about 2- and 3-fold in the presence of LVH and significant proteinuria, respectively. The probability of having sustained hypertension rather than WCH was about 10-fold greater in patients with contemporaneous LVH, significant proteinuria and CBP of 140 mmHg. The performance of model was adequate, as testified by the C-index of 0.757. We also fitted a model where only significant covariates were included; this reduced model showed similar odds ratio estimates and its performance was only slightly diminished (C-index: 0.740).
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The prevalence of patients treated with antihypertensive drugs and their mean number was reported in Table 2. The use of converting enzyme inhibitors and/or angiotensin receptor blockers was 86.8% in NOR, 62.5% in MH, 92.1% in WCH and 87.4% in SH (P = 0.015). Diuretics were administered in 39.5, 56.3, 67.4 and 59.1% of patients in the four groups, respectively (P = 0.06). Adherence to low-sodium diet (daily urinary sodium excretion
100 mEq/day) was significantly (P = 0.002) greater in patients with normal CBP (42.1 and 52.9% in NOR and MH patients, respectively) than in those with uncontrolled CBP (18.7 and 21.8% in WCH and SH groups, respectively). Erythropoietin treatment significantly differed in the four groups (0% in NOR, 6% in MH, 4% in WCH and 12% in SH, P = 0.031) |
Discussion |
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Optimal BP control is a main treatment goal to improve renal and cardiovascular prognosis in CKD patients [1,5,7–9]. However, the achievement of the systolic BP target recommended by International Guidelines (<130 mmHg) remains largely inadequate independently from the type of clinical referral [4,10–12]. In the CKD population, ABP has been suggested to be superior to CBP in predicting ESRD and death [14]. A further advantage of ABP measurement is represented by a more careful evaluation of hypertensive state. Indeed, by combining information from CBP and ABP, it is possible to disclose WCH that is the contemporaneous presence of high CBP and normal ABP. Detection of this condition may help physicians in correctly planning antihypertensive therapy in patients, such as those with CKD, that are at high risk of developing CV and renal damage from excessive BP reduction [7,16,18]. On the other hand, WCH may in part account for the strikingly high prevalence of uncontrolled hypertension in CKD despite regular follow-up in tertiary care and multidrug antihypertensive therapy [4,12].
This work provides first-time evidence that the dimension of WCH in CKD is relevant in Italy, as shown in the US by Agarwal and Andersen [13], being present in about one-third of the 290 patients examined. Consequently, if one considers the same BP target for office and ambulatory recordings, the prevalence of systolic BP <130 mmHg results more than two-times greater at ABP monitoring as compared with office BP measurement (47 vs 21%).
Indeed, the critical question raising from these findings is whether this large group of WCH patients should be treated to the same low BP goal generally indicated by guidelines for hypertensive CKD patients. This point is not trivial because the evidence for very aggressive BP reduction in CKD relies far more on epidemiological association and expert opinions in the Guidelines than trial evidence. Specifically, recent studies have demonstrated that systolic BP <110–120 mmHg in office is associated with increased risk for mortality and progression of CKD [7,16–18]. This study cannot answer to this question because of the cross-sectional design; nevertheless, it provides novel insights into this issue by examining the cardiovascular risk profile. WCH patients were characterized by a risk profile that was halfway between NOR and SH groups. This was testified not only by the systolic CBP levels, but also by the prevalence of diabetes and LVH. These data suggest that CKD patients with WCH are characterized by a considerable CV risk, that is definitely greater than that reported in WCH patients with essential hypertension [22–26]. This is not surprising because it is well known that CKD represents a risk factor negatively influencing mortality due to a clustering effect of the main CV risk factors [1]. This is further confirmed in a population-based study showing that CV burden is markedly greater in patients with low GFR when compared with those with more preserved renal function [27]. In addition, our WCH patients were also older than those with essential hypertension [23–26]. On this basis, WCH patients with impaired renal function should be treated intensively as SH patients. However, a recent study clearly demonstrated that among CKD patients with high CBP, those with a good control of ambulatory BP values (WCH) display a better cardiovascular and renal outcome as compared with patients with SH [14,15]. This observation supports the notion that even in patients with renal impairment ABP monitoring represents an essential tool not only for refining CV prognosis but also to correctly classify the hypertensive status. Combining office and ambulatory measurements, in fact, allows to identify WCH as a sub-class of hypertensive patients in whom intensification of antihypertensive treatment may be actually harmful. Indeed, as depicted in Figure 2, these patients display daytime and especially nighttime systolic BP values at the threshold limit of hypoperfusion (100 mmHg). Under these circumstances, therefore, intensification of antihypertensive therapy merely driven by systolic BP >130 mmHg in office may potentially expose patients to ischaemia-induced worsening of renal and cardiovascular outcome [7,16–18]. This problem becomes even more critical when considering that in WCH, nighttime diastolic BP reached the lowest value as compared with other groups; this finding deserves attention because recent studies in non-CKD patients with coronary artery disease have disclosed a J-shaped relationship between office diastolic BP and myocardial infarction [28].
In the past years, reimbursement issues, equipment expenses and time efforts to train patients in monitor use have limited a wider acceptance of ABP monitoring in routine clinical practice. This restriction can be overcome by determining the clinical factors that identify the ideal candidates to ABP monitoring. In the present study, the logistic regression analysis, performed in the 228 patients with high CBP, indicates that the simultaneous presence of systolic CBP >140 mmHg, LVH and significant proteinuria increases by 10 times the probability of having SH rather than WCH. This finding allows to identify the patients with high risk of having sustained hypertension on the basis of their clinical characteristics. In these SH patients, therefore, attainment of BP recordings by ABP likely becomes less important. This result has a clinical impact in terms of suggesting execution of ABP measurement only in the subgroup of CKD patients with lower CBP and minor cardio–renal damage in order to detect WCH. Restricting the indication of ABP monitoring mainly to these patients may reasonably reduce not only the economical costs for the healthcare system, engagement of physicians and the discomfort for patients, but also the risk of detrimental effects of cardio–renal ischaemia induced by over-treatment of BP.
The main limitation of this study is related to the cross-sectional design. This study cannot provide evidence, in fact, that differences in the global CV risk translate into a different outcome. However, BP, proteinuria and LVH are now widely recognized as the main factors influencing progression of cardiac and renal disease, and therefore are commonly used as surrogates of cardio–renal risk in CKD [1,5].
In conclusion, this cross-sectional analysis emphasizes the importance of ABP in CKD patients not only to refine prognosis but also to improve antihypertensive intervention. Indeed, we provide evidence from an unselected population that in patients with non-dialytic CKD stage 3–5, WCH is present approximately in one patient out of three and this finding should be taken into account when assessing BP control rates in CKD. ABP monitoring becomes critical to diagnose this phenomenon, especially in the absence of predictors of sustained hypertension, such as LVH, significant proteinuria and high clinical BP values, and to guide antihypertensive drug prescription. In the presence of WCH, in fact, intensification of antihypertensive therapy to reach a clinical BP target <130 mmHg may possibly increase the risk of renal and cardiac hypoperfusion.
Further prospective studies in CKD are certainly required to validate the protective effects on CV mortality of the recommended low BP target in office; nonetheless, our results support a wider use of ABP monitoring to allow a more proper evaluation of the relationship between hypertension control and cardio–renal outcome.
Conflict of interest statement. None declared.
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Accepted in revised form: 5. 3.07
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