epidemiological and observational studies indicate hypertension as a major cause of chronic kidney disease ( ckd ) .
in fact , hypertension and ckd are strongly connected because hypertension is both a cause and a consequence of ckd .
hypertensive patients with ckd present higher morbidity and mortality rates when compared with those with normal renal function [ 3 , 4 ] .
additionally , high blood pressure is a predictor of decline of glomerular filtration rate ( gfr ) , and conversely , adequate blood pressure control contributes to preserve renal function [ 57 ] .
vascular changes are commonly observed in ckd patients , including reduced arterial elasticity observed in patients with end - stage renal disease [ 8 , 9 ] .
fibroelastic intimal thickening , increased extracellular matrix , enhanced collagen density , and vascular calcification seem to contribute to stiffer arteries in ckd patients [ 10 , 11 ] .
it has been demonstrated that vascular stiffness may predict adverse cardiovascular outcomes [ 12 , 13 ] .
current gold standard for vascular stiffness evaluation is the pulse wave velocity ( pwv ) which requires complex equipment and therefore is not commonly used in clinical practice .
recently , a new parameter named ambulatory arterial stiffness index ( aasi ) was proposed for this evaluation [ 15 , 16 ] .
this index is derived from the regression slope of the diastolic on systolic blood pressure , using all of the readings during ambulatory blood pressure monitoring ( abpm ) .
it has already been reported that aasi presents good correlation with target organ damage and glomerular filtration rate ( gfr ) in essential hypertension [ 1720 ] . moreover
, aasi may also correlate with cardiovascular events and mortality [ 21 , 22 ] . on the other hand
, there have been few studies investigating this index in hypertensive patients with different stages of ckd .
the aim of our study was to evaluate the aasi in nondiabetic hypertensive patients with ckd and in those with normal renal function .
a case - control study involving 60 consecutive patients with primary hypertension was carried out in our institution .
hypertensive patients with ckd , aged 40 to 75 years and estimated glomerular filtration rate ( egfr ) < 60  ml / min by the modification of diet in renal disease ( mdrd ) equation , were included ( ckd group ) .
other 30 patients matched by age ( 2 years ) and gender with the ckd patients were selected from the hypertension outpatient clinic at the same institution .
these patients presented systemic arterial hypertension ( sah group ) and serum creatinine less than 1  mg / dl .
exclusion criteria were diabetes mellitus , hypertriglyceridemia ( > 400  mg / dl ) , urinary albumin - to - creatinine ratio ( uacr ) > 1000  mg / g , acute renal failure , renal replacement therapy , regular use of anti - inflammatory drugs , and history of myocardial infarction or cerebrovascular disease in the last 6 months .
the local ethics committee has previously approved the study protocol , and all participants gave written informed consent .
office blood pressure was obtained using an electronic device ( model hem-705cp , omron healthcare inc .
patients were seated for 30 minutes before measurement and refrained from smoking and caffeine ingestion in this period of time .
three readings , one minute apart , were done , and the average of these measurements was defined as the patient clinic blood pressure .
the patients underwent 24-hour abpm in nondominant arm with spacelabs 90207 monitor ( spacelabs inc . , redmond , wa , usa ) , validated by the british hypertension society and the association for the advancement of medical instrumentation protocol .
readings were taken every 20 minutes during the day and every 30 minutes at night .
the percentage decline in nocturnal blood pressure was calculated as follows for systolic ( sbp ) and diastolic ( dbp ) blood pressures : percentage decline in nocturnal blood pressure = ( daytime blood pressurenight - time blood pressure )  100/daytime blood pressure .
the aasi was calculated from 1 minus the regression slope of diastolic pressure on systolic blood pressure .
fasting venous blood was collected from participants to measure total cholesterol , triglycerides ( tg ) , high - density lipoprotein cholesterol ( hdl - c ) , glucose , creatinine ( enzymatic method ) , and uric acid .
the low - density lipoprotein cholesterol ( ldl - c ) level was calculated by the friedewald formula ( 8) .
egfr was assessed by modified mdrd equation : egfr = 0.741  175  cr  age( 0.742 if female ) .
c - reactive protein ( nephelometry , bn ii , siemens ag inc , munich , germany ) and morning urinary spot albumin and creatinine ( nephelometry , immage , beckman coulter inc , fullerton , ca , usa ) were also measured .
data are presented as mean  standard error of mean ( sem ) . for database management and statistical analyses , we used graphpad prism software , version 5.0 ( graphpad software inc . , ca , usa ) .
chi - squared test ( for 2  3 tables ) or fisher 's exact test ( for 2  2 tables ) and student 's t - test were used to compare proportions and means , respectively .
pearson 's correlation coefficients were used to explore associations between examined continuous variables with parametric distribution .
as expected , hemoglobin was significantly lower and serum creatinine and uric acid were significantly higher in ckd group ( table 1 ) .
mean egfr by mdrd in the ckd group was 35.3  2.8  ml / min .
c - reactive protein and uacr were significantly higher in ckd group ( table 1 ) .
the mean office and ambulatory blood pressure readings were similar in both groups ( table 2 ) , although ckd patients needed to use more antihypertensive drugs ( 2.7  0.2 versus 2.2  0.1 , p = 0.0398 ) to obtain blood pressure control . when ckd was compared to sah group concerning antihypertensive treatment , there was no significant difference for diuretics ( 60% versus 70% ) , angiotensin converting enzyme inhibitors / angiotensin receptor blockers ( 86% versus 77% ) and beta blockers ( 40% versus 37% ) . however , use of calcium channel antagonists was significantly more common in ckd patients ( 47% versus 23% , p < 0.01 ) .
the mean nocturnal systolic blood pressure fall was lower than 10% in both groups ( 4.0  1.5% in ckd versus 7.6  1.1% in sah , p = 0.0588 ) .
there were 40% of dipper patients , 50% of nondipper , and 10% of reverse dipper in sah group .
on the other hand , ckd group presented 30% of dipping pattern , 40% nondipping , and 30% reverse dipping ( figure 1 ) .
pulse pressure was not different between ckd and sah groups ( 54  2 versus 50  2  mmhg , p = 0.20 ) .
the aasi index was significantly higher in ckd patients when compared with sah group ( 0.45  0.03 versus 0.37  0.02 , p = 0.04 ) .
correlation tests showed that aasi was positively related to age ( r = 0.38 , p < 0.01 ) , pulse pressure ( r = 0.43 , p < 0.01 ) and inversely related to nocturnal blood pressure fall ( r = 0.28 , p = 0.03 ) ( figure 2 ) .
however , when egfr was analyzed among all patients , those with egfr less than 30  ml / min had higher aasi ( figure 3 ) .
the results of our study demonstrate that hypertensive patients with ckd presented a higher aasi when compared to those with normal renal function . supporting the concept that aasi is a marker of arterial stiffness , li et al .
moreover , in a cohort of 11,291 patients , dolan et al . showed that aasi carried prognostic information , as it was a predictor of stroke and cardiac death . in a japanese study ,
kikuya et al . also observed that aasi predicted cardiovascular and stroke mortality over and beyond pulse pressure .
demonstrated that aasi is a predictor of cardiovascular morbidity and mortality in 547 patients with resistant hypertension .
furthermore , some research groups have already reported that aasi presents good reproducibility , with repeatability coefficients close to 60% [ 26 , 27 ] .
criticizers say that this index is dependent on pulse pressure and dipping pattern and do not provide new information [ 28 , 29 ] .
schillaci et al . studied 515 untreated hypertensive patients and found that aasi was strongly dependent on the degree of nocturnal blood pressure fall and only weakly related to pulse wave velocity .
showed that aasi was positively related to urinary albumin excretion and negatively related to estimated creatinine clearance in a population of 168 patients with recently diagnosed hypertension and without drug treatment .
studied 142 hypertensive patients without drug treatment and with serum creatinine less than 1.5  mg / dl and demonstrated that patients with high aasi presented lower gfr .
this paper also suggested that aasi was a better predictor of gfr decline than 24 h pulse pressure . in 554 hypertensive patients with and without drug treatment , garcia - garcia et al . observed that aasi correlates with egfr , carotid intima - media thickness , and cornell voltage - duration product .
elderly people are predisposed to lose arterial elastic laminae and increase collagen deposits in vascular wall [ 10 , 31 ] . this way , assuming aasi as a marker of vascular stiffness
interestingly , ckd patients tend to have stiffer vessels when compared to age- and blood - pressure - matched patients with normal renal function [ 31 , 32 ] . beyond traditional risk factors , such as hypertension and dyslipidemia , uremia seems also play a role to this finding .
mineral metabolism alterations and arterial calcification are probably relevant mechanisms [ 10 , 33 ] .
this may be one hypothesis to explain why aasi was higher in ckd than in sah group despite similar office and ambulatory blood pressure measurements in the present study .
moreover , patients with the lowest egfr ( stage 4 , according to the american national kidney foundation ) presented higher aasi .
pulse pressure and nocturnal blood pressure fall are two parameters from abpm that correlate with arterial stiffness [ 34 , 35 ] .
. showed that hypertensive patients with nondipper pattern presented stiffer vessels when measured by pulse wave velocity , suggesting a relationship between blunted nocturnal blood pressure fall and reduced arterial elasticity [ 35 , 36 ] .
these findings corroborate with our study , since nocturnal blood pressure fall and pulse pressure were correlated with aasi .
. however , our data strongly implies the value of aasi as a noninvasive tool for hemodynamic evaluation of ckd patient and reinforces the role of abpm in hypertensive patients with renal dysfunction . increased aasi might be one of the pathophysiological changes observed in ckd patients before the progression to end stage renal disease .
more studies are needed to support the clinical usefulness of this parameter , but we propose that the software for abpm analysis should include aasi value as a marker of cardiovascular risk assessment in the near future .
 ambulatory arterial stiffness index ( aasi ) is a parameter obtained from ambulatory blood pressure monitoring ( abpm ) that correlates with clinical endpoints . 
 the aim of this study was to compare aasi in nondiabetic hypertensive patients with and without chronic kidney disease ( ckd ) . 
 subjects with systemic arterial hypertension ( sah , n = 30 ) with normal renal function , aged 40 to 75 years , were compared to hypertensive patients with ckd ( n = 30 ) presenting estimated glomerular filtration rate ( egfr ) < 60  ml / min by mdrd formula . 
 abpm was carried out in all patients . in ckd group , 
 egfr was 35.3  2.8  ml / min . 
 the mean 24-hour systolic and diastolic blood pressure ( bp ) was similar in both groups . 
 aasi was significantly higher in ckd group ( 0.45  0.03 versus 0.37  0.02 , p < 0.05 ) , positively correlated to age ( r = 0.38 , p < 0.01 ) and pulse pressure ( r = 0.43 , p < 0.01 ) and negatively correlated to nocturnal bp fall ( r = -0.28 , p = 0.03 ) . 
 these findings indicate the presence of stiffer vessels in ckd hypertensive patients . 
1. Introduction
2. Methods
3. Results
4. Discussion