BACKGROUND: Evidence for the influence of ambulatory blood pressure on prognosis derives mainly from population-based studies and a few relatively small clinical investigations. This study examined the associations of blood pressure measured in the clinic (clinic blood pressure) and 24-hour ambulatory blood pressure with all-cause and cardiovascular mortality in a large cohort of patients in primary care. METHODS: We analyzed data from a registry-based, multicenter, national cohort that included 63,910 adults recruited from 2004 through 2014 in Spain. Clinic and 24-hour ambulatory blood-pressure data were examined in the following categories: sustained hypertension (elevated clinic and elevated 24-hour ambulatory blood pressure),

Recent data suggest that visit-to-visit variability of blood pressure (BP) is associated with cardiovascular events. We evaluated the role of BP variability as a determinant of end-stage renal disease (ESRD). Using nationally representative data from the Korean National Health Insurance System, 8 199 089 subjects had been enrolled during 2009 to 2010 who were free of ESRD and underwent >/=3 health examinations during 2005 to 2010 were followed to the end of 2017. BP variability was measured using the coefficient of variation, SD, and variability independent of the mean. The primary outcome was the development of ESRD, defined as a combination of the relevant disease code and the initiation of renal replacement therapy. The chi(2) test, t test, and log-rank test were used in the statistical analysis. There were 16 567 cases of ESRD during a median follow-up of 7.89+/-0.88 years. The highest quartile of systolic or diastolic BP showed a higher incident rate of ESRD compared with the other 3 quartiles. It was augmented in patients with the highest quartile of both systolic and diastolic BP variabilities. Among patients with the highest quartile of systolic and diastolic BP variabilities, the uncontrolled hypertension group (>140/90 mm Hg) taking antihypertensive medication showed the highest incidence rate of ESRD. These results were consistent when modeling variability of BP using coefficient of variation, SD, and variability independent of the mean and in various sensitivity analyses. Systolic and diastolic BP variabilities were independently associated with an increased incidence of ESRD, and it was augmented when both variabilities were present together.

BACKGROUND: Analyses of some randomised trials show that calcium-channel blockers reduce the risk of stroke more than expected on the basis of mean blood pressure alone and that beta blockers are less effective than expected. We aimed to investigate whether the effects of these drugs on variability in blood pressure might explain these disparities in effect on stroke risk. METHODS: The Anglo-Scandinavian Cardiac Outcomes Trial Blood Pressure Lowering Arm (ASCOT-BPLA) compared amlodipine-based regimens with atenolol-based regimens in 19 257 patients with hypertension and other vascular risk factors and the Medical Research Council (MRC) trial compared atenolol-based and diuretic-based regimens versus placebo in 4396 hypertensive patients aged 65-74 years. We expressed visit-to-visit variability of blood pressure during follow-up in the two trials as standard deviation (SD) and as transformations uncorrelated with mean blood pressure. For ASCOT-BPLA, we also studied within-visit variability and variability on 24 h ambulatory blood-pressure monitoring (ABPM). RESULTS: In ASCOT-BPLA, group systolic blood pressure (SBP) SD was lower in the amlodipine group than in the atenolol group at all follow-up visits (p<0.0001), mainly because of lower within-individual visit-to-visit variability. Within-visit and ABPM variability in SBP were also lower in the amlodipine group than in the atenolol group (all p<0.0001). Analysis of changes from baseline showed that variability decreased over time in the amlodipine group and increased in the atenolol group. The lower risk of stroke in the amlodipine group (hazard ratio 0.78, 95% CI 0.67-0.90) was partly attenuated by adjusting for mean SBP during follow-up (0.84, 0.72-0.98), but was abolished by also adjusting for within-individual SD of clinic SBP (0.99, 0.85-1.16). Findings were similar for coronary events. In the ABPM substudy, reduced variability in daytime SBP in the amlodipine group (p<0.0001) partly accounted for the reduced risk of vascular events, but reduced visit-to-visit variability in clinic SBP had a greater effect. In the MRC trial, group SD SBP and all measures of within-individual visit-to-visit variability in SBP were increased in the atenolol group compared with both the placebo group and the diuretic group during initial follow-up (all p<0.0001). subsequent="" temporal="" trends="" in="" variability="" in="" blood="" pressure="" during="" follow-up="" in="" the="" atenolol="" group="" correlated="" with="" trends="" in="" stroke="" risk.="" interpretation:="" the="" opposite="" effects="" of="" calcium-channel="" blockers="" and="" beta="" blockers="" variability="" of="" blood="" pressure="" account="" for="" the="" disparity="" in="" observed="" effects="" risk="" of="" stroke="" and="" expected="" effects="" based="" mean="" blood="" pressure.="" to="" prevent="" stroke="" most="" effectively="" blood-pressure-lowering="" drugs="" should="" reduce="" mean="" blood="" pressure="" without="" increasing="" variability="" ideally="" they="" should="" reduce="" both.="">

In the past, endothelium was thought to be only a mechanical barrier. Today, endothelium is known to be a tissue regulating vascular tone, cell growth and the interaction between the leukocytes, thrombocytes and the vessel wall. It also synthesizes growth factors and thrombo-regulatory molecules and responds to physical and chemical signals. Even though the term

Left atrial function has an important role in determining optimal performance of the heart. Increase of left atrial dysfunction and volume are poor prognostic factors. In this study, we investigated independent determinants of left atrial function in non-diabetic patients with de novo hypertension. The study included 124 consecutive non-diabetic patients with de novo hypertension. Brachial artery flow-mediated dilatation, carotid intima-media thickness, transthoracic echocardiography, 24-h rhythm holter, and aortic stiffness measurements were recorded. In echocardiography, left atrial maximum (LAMaV) and minimum (LAMiV) volumes were calculated. Left atrium total emptying fraction (LATEF) and total emptying volume (LATEV) were divided into two groups according to the mean levels. Multivariate analysis was performed after correlation analysis for LATEV and LATEF mean levels. By logistic regression analysis, systolic blood pressure (OR 0.882, 95% CI 0.784-0.992, p = 0.036), percent of flow-mediated dilation (OR 0.747, 95% CI 0.595-0.938, p = 0.012), and presence of carotid plaque (OR 0.014, 95% CI 0.001-0.188, p = 0.001) were found as independent variables that determine LATEF. Age (OR 0.879, 95% CI 0.795-0.972, p = 0.012), smoking (OR 23.739, 95% CI 2.699-208.810, p = 0.004), left ventricular mass index (OR 1.052, 95% CI 1.012-1.094, p = 0.011), mitrale E-wave velocity (OR 1.108, 95% CI 1.031-1.191, p = 0.005) and LDL (low-density lipoprotein) cholesterol (OR 0.942, 95% CI 0.911-0.974, p = 0.001) were independent predictors of LATEV. In non-diabetic patients with de novo hypertension endothelial dysfunction, subclinical atherosclerosis and LDL cholesterol levels independently affect left atrial function.

The target organs damage in hypertension is mainly realized through an endothelial dysfunction. The present study investigated the inflammatory and endothelial dysfunction's biomarkers in patients with hypertension before and after the achieving the target level of blood pressure. We've performed clinical and laboratory study of 44 patients (17 men, 27 women, mean age 58.59 +/- 10.57 years) with the hypertension stage II, degrees2-3, high and very high risk of cardiovascular complications, not reaching the target level of blood pressure at the previous therapy. All patients received standardized therapy with a fixed combination of amlodipine / indapamide / perindopril in an individually selected dosage. The duration of the follow-up was 6 months. The levels of pro-inflammatory interleukin-6 (IL-6), anti-inflammatory interleukin-10 (IL-10), vascular cell adhesion molecule-1 (sVCAM-1) and vasculoendothelial growth factor (VEGF) were measured. All patients achieved the target blood pressure level at the end of the study (systolic blood pressure was 125.1 +/- 6.9 mm Hg, diastolic - 82.2 +/- 5 mm Hg, p < 0.001). After 6 months, there was no significant dynamics of inflammatory biomarkers. The level of sVCAM-1, as an indicator of endothelial dysfunction, decreased (898.67 +/- 433.5 ng / ml vs. 1063.5 +/- 442.4 ng / ml at the start of treatment, p < 0.001.="" thus="" it="" is="" possible="" to="" use="" vascular="" cell="" adhesion="" molecule-1="" as="" a="" biomarker="" of="" endothelial="" dysfunction="" in="" patients="" with="" hypertension.="" adequate="" therapy="" of="" hypertension="" with="" achievement="" of="" target="" blood="" pressure="" levels="" improves="" vascular="" endothelial="" function="" significantly="" reducing="" svcam-1="" expression.="">

The aim of this study was to investigate the relationship between endothelin-1, nitric oxide, insulin resistance, and blood pressure in young subjects with a high prevalence of excess weight and/or elevated blood pressure. In a cohort of 238 children (mean age = 11.1 years), height, weight, waist circumference, and blood pressure were assessed. Body mass index, waist-to-height ratio, and blood pressure percentiles were calculated, and the children were classified as having excess weight and elevated blood pressure according to the International Obesity Task Force and the US blood pressure nomograms specific for gender, age and height, respectively. Endothelin-1 and nitric oxide production were assessed, and the homeostatic model assessment index was calculated. Forty-three percent of children were male, 71% had excess weight, and 37% had systolic and/or diastolic values above the ninetieth percentile. Plasma endothelin-1 and nitric oxide production were independently correlated (p < 0.05.="" in="" multivariate="" analyses="" the="" homa="" index="" was="" associated="" with="" systolic="" and="" diastolic="" blood="" pressure="" p="0.01)," and="" nitric="" oxide="" was="" independently="" related="" to="" diastolic="" blood="" pressure="" p="0.04)," even="" after="" adjustment="" for="" measures="" of="" body="" composition.="" by="" using="" the="" waist-to-height="" ratio="" instead="" of="" bmi="" in="" the="" statistical="" model="" the="" association="" between="" the="" homeostatic="" model="" assessment="" index="" and="" blood="" pressure="" was="" attenuated="" while="" the="" results="" remained="" similar="" for="" nitric="" oxide.="" no="" correlation="" was="" found="" between="" endothelin-1="" and="" blood="" pressure.="" in="" our="" study="" population="" the="" correlation="" between="" nitric="" oxide="" and="" blood="" pressure="" and="" the="" lack="" of="" a="" relationship="" between="" endothelin-1="" and="" blood="" pressure="" could="" be="" explained="" by="" an="" increase="" in="" the="" vasodilator="" effect="" of="" local="" and="" systemic="" nitric="" oxide="" which="" counteracts="" the="" possible="" hypertensive="" effect="" of="" endothelin-1.="">

BACKGROUND: Damage to the endothelium due to ischemia reperfusion injury (IRI) leads to a disruption of the microvasculature, which could be influenced by angiopoietin 1 via its effects on endothelium. We investigated the physiological and therapeutic roles of angiopoietin 1 in renal IRI using angiopoietin 1 knockout and over-expression mice. METHODS: Renal IRI was induced by clamping the right renal artery seven days after left uninephrectomy for 25 min followed by reperfusion. A whole body angiopoietin 1 knockout was achieved by induction with tamoxifen. The renal tubule over-expression of angiopoietin 1 was induced by doxycycline. RESULTS: In the normal mice, the renal expression of angiopoietin 1 increased 7 days to 14 days after IRI. The angiopoietin 1 knockout caused a delay in the recovery of renal function, less tubular regeneration and more residual tubular necrosis. The endothelial density was lower and the VE-cadherin protein loss was greater in the knockout mice. The over-expression of angiopoietin 1 attenuated the tubular necrosis and renal function impairment 1 and 3 days after IRI. The loss of the endothelium was ameliorated in the over-expression mice. This protective effect was associated with the up-regulation of the gene expression of epidermal growth factor, hepatocyte growth factor, and insulin like growth factor-1 and less tubular apoptosis. The over-expression of angiopoietin 1 stimulated tumor necrosis factor-alpha, C-C chemokine receptor type 2 and CX3C chemokine receptor 1 inflammatory gene expression, but did not influence macrophage infiltration. CONCLUSIONS: Altogether, the augmentation and downregulation of angiopoietin 1 attenuated renal damage and impaired renal recovery, respectively, by influencing the survival/regeneration of the endothelium. The manipulation of angiopoietin 1 represents a novel therapeutic approach for the treatment of ischemic kidney injury.

Endothelium-derived endothelin (ET)-1 has been implicated in the development of hypertension and end-organ damage, but its exact role remains unclear. We have shown that tamoxifen-inducible endothelium-restricted human ET-1 overexpressing (ieET-1) mice exhibited blood pressure rise after a 3-week induction in an ET type A (ETA) receptor-dependent manner, in absence of vascular and renal injury. It is unknown whether long-term ET-1 overexpression results in sustained blood pressure elevation and vascular and renal injury. Adult male ieET-1 and control tamoxifen-inducible endothelium-restricted Cre recombinase (ieCre) mice were induced with tamoxifen and 2.5 months later, were treated with or without the ETA receptor blocker atrasentan for 2 weeks. Three-month induction of endothelial human ET-1 overexpression increased blood pressure (P<0.01), reduced renal artery flow (P<0.001), and caused mesenteric small artery stiffening (P<0.05) and endothelial dysfunction (P<0.01). These changes were accompanied by enhanced mesenteric small artery Col1A1 and Col3A1 expression, and perivascular adipose tissue oxidative stress (P<0.05) and monocyte/macrophage infiltration (P<0.05). Early renal injury was demonstrated by increased kidney injury molecule-1 expression in renal cortex tubules (P<0.05), with, however, undetectable lesions using histochemistry staining and unchanged urinary albumin. There was associated increased myeloid (CD11b(+)) and myeloid-derived suppressive cell (CD11b(+)Gr-1(+)) renal infiltration (P<0.01) and greater frequency of myeloid and renal cells expressing the proinflammatory marker CD36 (P<0.05). Atrasentan reversed or reduced all of the above changes (P<0.05) except="" the="" endothelial="" dysfunction="" and="" collagen="" expression="" and="" reduced="" renal="" artery="" flow.="" these="" results="" demonstrate="" that="" long-term="" exposure="" to="" endothelial="" human="" et-1="" overexpression="" causes="" sustained="" blood="" pressure="" elevation="" and="" vascular="" and="" renal="" injury="" via="" eta="" receptors.="">

Background Endothelial NO synthase plays a central role in regulating vasodilation and blood pressure. Intracellular Ca(2+) mobilization is a critical modulator of endothelial NO synthase function, and increased cytosolic Ca(2+) concentration in endothelial cells is able to induce endothelial NO synthase phosphorylation. Ca(2+) release mediated by 3 subtypes of inositol 1,4,5-trisphosphate receptors ( IP 3Rs) from the endoplasmic reticulum and subsequent Ca(2+) entry after endoplasmic reticulum Ca(2+) store depletion has been proposed to be the major pathway to mobilize Ca(2+) in endothelial cells. However, the physiological role of IP 3Rs in regulating blood pressure remains largely unclear. Methods and Results To investigate the role of endothelial IP 3Rs in blood pressure regulation, we first generated an inducible endothelial cell-specific IP 3R1 knockout mouse model and found that deletion of IP 3R1 in adult endothelial cells did not affect vasodilation and blood pressure. Considering all 3 subtypes of IP 3Rs are expressed in mouse endothelial cells, we further generated inducible endothelial cell-specific IP 3R triple knockout mice and found that deletion of all 3 IP 3R subtypes decreased plasma NO concentration and increased basal blood pressure. Furthermore, IP 3R deficiency reduced acetylcholine-induced vasodilation and endothelial NO synthase phosphorylation at Ser1177. Conclusions Our results reveal that IP 3R-mediated Ca(2+) release in vascular endothelial cells plays an important role in regulating vasodilation and physiological blood pressure.

BACKGROUND AND AIMS: Arterial wall viscosity (AWV) is regulated by endothelium-derived NO and epoxyeicosatrienoic acids (EETs) under baseline physiological conditions. Whether these factors regulate AWV during blood flow increase and whether this mechanism is affected in essential hypertensive patients (HT) remain unknown. METHODS: The evolution of radial artery diameter, wall thickness and arterial pressure in response to an increase in flow induced by hand skin heating were measured in 18 untreated HT and 14 normotensive controls (NT) during local infusion of saline and the respective pharmacological inhibitors of NO-synthase and EETs synthesis by cytochrome P450, L-NMMA and/or fluconazole. AWV was estimated by the ratio of the viscous energy dissipated (WV) to the elastic energy stored (WE) obtained from the pressure-diameter relationship. Concomitant changes in operating conditions, which influence the AWV, were taken into account by calculating the midwall stress. RESULTS: Baseline WV and WE were higher in HT than in NT but WV/WE was similar. In saline condition, WV/WE increased in HT during heating but not in NT. In the presence of L-NMMA and/or fluconazole, WV/WE increased during heating in NT. In contrast, these inhibitors did not modify the increase in WV/WE during heating in HT compared to saline. In all conditions, a larger increase in WV than WE was responsible for the increase in WV/WE. CONCLUSIONS: The release of NO and EETs maintains a stable AWV during flow increase and this endothelial adaptive regulation is lost during essential hypertension, which may promote excessive viscous energy dissipation and cardiovascular uncoupling. Restoration of EETs availability with inhibitors of soluble epoxide hydrolase could thus constitute a promising pharmacological approach to restore the endothelial adaptive regulation of AWV.

BACKGROUND: Biomarkers of oxidative stress (OS) are involved in the pathophysiology of hypertension (HTN) and endothelial dysfunction is also related to HTN. Still, a significant association of OS, as well as endothelial function, remains unclear in HTN. METHODS: Totalling 222 North Indian peoples aged 18-80 participated in the study. Of these participants, 74 were elderly hypertensive subjects (age >/=60 years), and 128 were normotensive subjects (age >/=60 years-control I; n = 74, and <60 years-control="" ii="" n="74)." os="" was="" assessed="" by="" measurement="" of="" total="" oxidant="" status="" tos="" and="" total="" antioxidant="" status="" tas="" using="" a="" colorimetric="" and="" automated="" method="" developed="" by="" erel="" o.="" endothelial="" dysfunction="" was="" assessed="" by="" measurement="" of="" flow-mediated="" dilation="" fmd="" using="" doppler="" ultrasound="" system.="" results:="" tos="" and="" osi="" were="" significantly="" increased="" and="" tas="" and="" fmd="" significantly="" decreased="" in="" patients="" with="" htn="" as="" compared="" to="" control="" i="" and="" control="" ii.="" the="" increase="" in="" the="" level="" of="" tos="" and="" a="" decrease="" in="" the="" level="" of="" tas="" and="" fmd="" were="" also="" evident="" with="" advancing="" age.="" fmd="" was="" negatively="" correlated="" with="" tos="" and="" positively="" correlated="" with="" tas.="" conclusion:="" decreased="" tas="" level="" increased="" tos="" level="" reflect="" os="" that="" may="" be="" the="" reason="" for="" reduced="" fmd="" in="" elderly="" hypertensive="" patients.="">

Background: Neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR) are associated with worse outcome in various diseases. Non-dipping blood pressure pattern is associated with higher cardiovascular mortality. The aim of this study was to explore the association between NLR and PLR in patients with dipper versus non-dipper hypertension.
Methods: The study included 166 patients with hypertension. Eighty-three patients (40 male, mean age: 49.1 +/- 10.5 years) had dipper hypertension, while 83 patients (41 male, mean age: 52.3 +/- 12.7 years) had non-dipper hypertension.
Results: Baseline demographic characteristics were similar in both groups. Patients with non-dipper hypertension had significantly higher NLR compared to dipper hypertension (2.3 +/- 0.9 versus 1.8 +/- 0.5, p < 0.001). Patients with non-dipper hypertension had significantly higher PLR compared to dipper hypertension (117.7 +/- 35.2 versus 100.9 +/- 30.5, p = 0.001). In univariate analysis, hyperlipidemia, smoking, presence of diabetes, PLR more than 107 and NLR more than 1.89 were among predictors of dipper and non-dipper status. In logistic regression analyses, only hyperlipidemia (odds ratio: 2.96, CI: 1.22-7.13) and PLR more than 107 (odds ratio: 2.62, Cl: 1.13-6.06) were independent predictors of dipper and non-dipper status. A PLR of 107 or higher predicted non-dipper status with a sensitivity of 66.3% and specificity of 68.7%.
Conclusion: We demonstrated that patients with non-dipper hypertension had significantly higher NLR and PLR compared to dipper hypertension, which has not been reported previously. Moreover PLR more than 107 but not NLR was independent predictor of non-dipper status.

Immune cells infiltrate the kidney, vasculature, and central nervous system during hypertension, consequently amplifying tissue damage and/or blood pressure elevation. Mononuclear cell motility depends partly on chemokines, which are small cytokines that guide cells through an increasing concentration gradient via ligation of their receptors. Tissue expression of several chemokines is elevated in clinical and experimental hypertension. Likewise, immune cells have enhanced chemokine receptor expression during hypertension, driving immune cell infiltration and inappropriate inflammation in cardiovascular control centers. T lymphocytes and monocytes/macrophages are pivotal mediators of hypertensive inflammation, and these cells migrate in response to several chemokines. As powerful drivers of diapedesis, the chemokines CCL2 and CCL5 have long been implicated in hypertension, but experimental data highlight divergent, context-specific effects of these chemokines on blood pressure and tissue injury. Several other chemokines, particularly those of the CXC family, contribute to blood pressure elevation and target organ damage. Given the significant interplay and chemotactic redundancy among chemokines during disease, future work must not only describe the actions of individual chemokines in hypertension, but also characterize how manipulating a single chemokine modulates the expression and/or function of other chemokines and their cognate receptors. This information will facilitate the design of precise chemotactic immunotherapies to limit cardiovascular and renal morbidity in hypertensive patients.

INTRODUCTION: Unexplained differences between classes of antihypertensive drugs in their effectiveness in preventing stroke might be due to class effects on intraindividual variability in blood pressure. We did a systematic review to assess any such effects in randomised controlled trials. METHODS: Baseline and follow-up data for mean (SD) of systolic blood pressure (SBP) were extracted from trial reports. Effect of treatment on interindividual variance (SD2) in blood pressure (a surrogate for within-individual variability), expressed as the ratio of the variances (VR), was related to effects on clinical outcomes. Pooled estimates were derived by use of random-effects meta-analysis. FINDINGS: Mean (SD) SBP at follow-up was reported in 389 (28%) of 1372 eligible trials. There was substantial heterogeneity between trials in VR (p<1 x 10(-40)), 68% of which was attributable to allocated drug class. Compared with other drugs, interindividual variation in SBP was reduced by calcium-channel blockers (VR 0.81, 95% CI 0.76-0.86, p<0.0001) and non-loop diuretic drugs (0.87, 0.79-0.96, p=0.007), and increased by angiotensin-converting enzyme (ACE) inhibitors (1.08, 1.02-1.15, p=0.008), angiotensin-receptor blockers (1.16, 1.07-1.25, p=0.0002), and beta blockers (1.17, 1.07-1.28, p=0.0007). Compared with placebo only, interindividual variation in SBP was reduced the most by calcium-channel blockers (0.76, 0.67-0.85, p<0.0001). Effects were consistent in parallel group and crossover design trials, and in analyses of dose-response. Across all trials, effects of treatment on VR of SBP (r2=0.372, p=0.0006) and on mean SBP (r2=0.328, p=0.0015) accounted for effects on stroke risk (eg, odds ratio 0.79, 0.71-0.87, p<0.0001, for VR< or="0.80)," and="" both="" remained="" significant="" in="" a="" combined="" model.="" interpretation:="" drug-class="" effects="" interindividual="" variation="" in="" blood="" pressure="" can="" account="" for="" differences="" in="" effects="" of="" antihypertensive="" drugs="" risk="" of="" stroke="" independently="" of="" effects="" mean="" sbp.="" funding:="" none.="">

BACKGROUND: Visit-to-visit variability of systolic blood pressure (SBP) has been shown to contribute to cardiovascular events and all-cause mortality. However, little is known about its long-term effect on renal function. We aim to examine the relationship between visit-to-visit blood pressure variability (BPV) and decline in renal function in patients with hypertension and to determine the level of systolic BPV that is associated with significant renal function decline. METHODS AND RESULTS: This is a 15-year retrospective cohort study of 825 hypertensive patients. Blood pressure readings every 3 months were retrieved from the 15 years of clinic visits. We used SD and coefficient of variation as a measure of systolic BPV. Serum creatinine was captured and estimated glomerular filtration rate was calculated at baseline, 5, 10, and 15 years. The mean SD of SBP was 14.2+/-3.1 mm Hg and coefficient of variation of SBP was 10.2+/-2%. Mean for estimated glomerular filtration rate slope was -1.0+/-1.5 mL/min per 1.73 m(2) per year. There was a significant relationship between BPV and slope of estimated glomerular filtration rate (SD: r=-0.16, P<0.001; coefficient of variation: r=-0.14, P<0.001, pearsons="" correlation.="" bpv="" of="" sbp="" for="" each="" individual="" was="" significantly="" associated="" with="" slope="" of="" estimated="" glomerular="" filtration="" rate="" after="" adjustment="" for="" mean="" sbp="" and="" other="" confounders.="" the="" cutoff="" values="" estimated="" by="" the="" receiver="" operating="" characteristic="" curve="" for="" the="" of="" chronic="" kidney="" disease="" for="" sd="" of="" sbp="" was="" 13.5="" mm="" hg="" and="" coefficient="" of="" variation="" of="" sbp="" was="" 9.74.="" conclusions:="" long-term="" visit-to-visit="" variability="" of="" sbp="" is="" an="" independent="" determinant="" of="" renal="" deterioration="" in="" patients="" with="" hypertension.="" hence="" every="" effort="" should="" be="" made="" to="" reduce="" bpv="" in="" order="" to="" slow="" down="" the="" decline="" of="" renal="" function.="">