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 ,:	Association of brachial artery measures with estimated GFR>60ml/min/1.73m2 in a cross-sectional study of the community-based women
Abstract
Objective: The purpose of this study is to estimate whether early decline in kidney disease is correlated with brachial artery measures as surrogate markers of the endothelial function in community-based women. 
Methods: We studied 36 women with estimated glomerular filtration rate (eGFR)>60 ml/min/1.73m2 in community-based population women were enrolled in this study. Brachial artery measures including flow-mediated vasodilation (FMD), nitroglycerin-mediated vasodilation (NMD), brachial artery diameter (BAD), FMD/NMD ratio and post-nitroglycerin brachial artery diameter (P-NTGD) examinations were measured in all subjects by using brachial artery ultrasonography. The eGFR was calculated using the Japanese GFR inference formula, which was developed by the Japanese Society of Nephrology. 
Results: There was significantly positive correlation between eGFR and FMD (r= 0.348, p=0.041), positive correlation between eGFR and FMD/NMD ratio (r=0.471, p=0.004) and negative correlation between eGFR and P-NTGD (r=-0.405, p=0.016) were recognized. Negative correlation between serum uric acid (SUA) and eGFR (r=-0.335, p=0.049) and negative correlation between FMD and SUA (r=-0.34, p=0.045) were also demonstrated. 
Conclusion: Mild renal dysfunction with eGFR>60ml/min/1.73m2 was associated with endothelial dysfunction in women. The cardio-renal interrelationship may be also suggested under mild renal dysfunction. We will indicate that mild renal dysfunction may be considered as a cardiovascular disease (CVD) risk factor, especially in women. 
Key words Estimated glomerular filtration rate�0Flow-mediated vasodilation�0Endothelial dysfunction�0Cardio-renal interrelationship�0Mild renal dysfunction00000000000 
00


Introduction
 Flow-mediated vasodilation (FMD), an endothelium-dependent function, and nitroglycerin-mediated vasodilation (NMD), an endothelium-independent function in the brachial artery is potent procedure for assessing vascular endothelial and vascular smooth muscle cell (VSMC) function [1]. Patients with severe chronic kidney disease (CKD) have high risk of occurring cardiovascular disease (CVD) [2], but it has been reported that subjects with mild kidney dysfunction have also an increased CVD risk in the community-based study [3]. It has been suggested that the increased risk of CVD has been contributed not only to clustering of CV risk factors [4] but also to endothelial dysfunction [5,6] in subjects with CKD. Though the threshold eGFR at which CV risk increases is unclear, expert consensus have proposed a level of < 60ml/min/1.73m2 [7] Studies have been reported that eGFR is associated with endothelial dysfunction in the community-based subjects [6, 8-11]. With regard to the restricting analysis to subject with eGFR>60ml/min/1.73m2 representing CKD stage 0-2, a few reports has been reported [9-11]. The cardio-renal interrelationship has been suggested under normal conditions [12]. It has been also reported that endothelial dysfunction is considered as one of the major pathophysiological mechanism contributing to the relation of CVD and CKD [6,13,14]. We think that early detection of cardio-renal interaction damage can contribute to the prevention of initiation or precipitation of diseases. According to the experts consensus proposed as a threshold of eGFR>60ml/min/1.73m2, we evaluate whether early decline in kidney function with eGFR>60 ml/min/1.73m2 value is correlated with brachial artery measures including FMD, FMD/NMD ratio and P-NTGD as indicators of reflecting the endothelial function. Except the relationship between endothelial dysfunction and eGFR value, serum uric acid (SUA) is an independent predictor of future development of CKD in subject with eGFR>60ml/min/1.73m2 [15,16]. Meanwhile, experimental study indicate that hyperuricemia cause systemic and glomerular hypertension, leading to endothelial dysfunction and experimental hyperuricemia also contribute to an afferent renal arteriopathy and tubulointerstitial fibrosis in the kidney [17-20]. It is plausible that elevated SUA may contribute to endothelial dysfunction, inflammation, oxidative stress and renin-angiotensin system (RAS) activation and leading to systemic atherosclerosis and/or reduced eGFR, namely, initiation and progression of CKD. We also add the estimation whether eGFR>60ml/min/1.73m2 of renal function is related with SUA. Furthermore, the evidence of SUA to stimulate oxidant production has already been studied in both adipocytes [21] and vascular smooth muscle cells (VSMC) [22]. In addition to these studies, Yu et al [23] have reported a mechanism of uric acid-induced human umbilical vein endothelial dysfunction. Clinical studies have also indicated the relationship between SUA and endothelial dysfunction [24-27]. Therefore, we have studied whether interrelationship among mild renal dysfunction assessed as estimated by eGFR.60ml/min/1.73m2, endothelial dysfunction examined by FMD and SUA as a risk factor of CVD and CKD are demonstrated. Meanwhile, carotid IMT is a marker to assess the largely medial hypertrophy of the vessel [28] and baPWV is a predictor to evaluate arterial stiffness [13]. In addition to the endothelial function, we added the examinations whether eGFR>60ml/min/1.73m2 value is correlated with different arterial trees at different sites. 

Materials and Methods
Study population
 Thirty six women with eGFR>60ml/min/1.73m2 renal function in community-based population were enrolled in this study (including: 11 cerebral infarction, 10 migraine, 3 cervical spondylosis, and 18 not otherwise). Thirty six subjects who fulfilled eGFR>60ml/min/1.73m2 value were enrolled in the study between March 2008 and April 2014. All vasoactive medications were withheld for at least a few days. Women patients were allowed to perform ultrasonographic examinations either in luteal or follicular phase. For the FMD examination, patients fasted for 12 hours before the study and they were studied in a quiet, temperature-controlled room. 

Vascular Reactivity
 FMD of the brachial artery was determined using high resolution B-mode ultrasonographic system (UNEXEX 18G, Japan) with a linear transducer midfrequency of 7.5MHz, using the technique described previous report [29, 30] Briefly, this was followed by inflation pneumatic tourniquet of placed around forearm to higher pressure 50mmHg more than systolic blood pressure and followed by deflation after 5 minutes. The scan was made by the procedure of autocalculation. Fifteen minutes were then allowed for vessel recovery and a further scan at rest was then recorded. An exogenous NO donor, such as a single high dose (0.3mg) of NTG spray has been given to determine the maximum obtainable vasodilator response, and to serve as a measure of endothelium-independent vasodilation reflecting VSMC function, in accordance with the previous report [1,29, 30]. Parameters including FMD, NMD and P-NTGD were expressed as previously described [29,30].

Carotid ultrasonography
The intima-media thickness (IMT) of the bilateral common carotid arteries (CCA) was measured by ultrasonography with a 10-MHz probe using an ultrasound system (Aplio SSA-700A, Toshiba Medical System, Tochigi, Japan). Measurement of IMT were performed on the visible CCA in either the near or the far wall, and maximum IMT was defined as IMT-C max. Measurement IMT were also made within a region free of plaque as previously described [28,29]. 

Brachial-ankle pulse wave velocity (baPWV) measurement 

baPWV was measured using a volume-plethysmographic apparatus (form PWV/ABI; Colin, Co.,Ltd., Komaki, Japan) and ankle- brachial pressure index (ABI) is measured simultaneously by these machines in accordance with a described method [29,31]

Statistical analysis 
 Numerical variables were expressed as mean�SD. Spearman�s bivariable correlation analysis was used to test the relationships between the numerical variables when appropriate. Statistical significance was defined as a p value of less than 0.05. The statistical analyses were performed using the SPSS software package (version 16.0; SPSS Inc., Chicago, IL). 
Results 
Baseline characteristics of study population are summarized in (Table 1). Mean age of the participants was 55.4�14.4 years (range: 19 to 80 years). 
Brachial artery measures of the participants were presented (Table 2). 
Table 3 shows Spearman�s rank correlation coefficients of the brachial artery measures in participants. FMD% was significantly correlated with FMD/NMD ratio (r=0.68. p<0.001). Significant correlation between FMD% and P-NTGD was recognized (r=--0.37, p=0.03).
Table 4 shows Spearman�s rank correlation coefficients of the atherosclerotic parameters in participants. Negative correlation between FMD and rt IMT (r=-0.664, p<0.001) and negative correlation between FMD and lt IMT (r=-0.546, p=0.005) were also detected. Positive correlation between rt IMT and rt baPWV (r=0.432, p=0.027), positive correlation between rt IMT and lt baPWV (r=0.478, p=0.010), positive correlation between lt IMT and rt baPWV (r=0.498, p=0.010) and positive correlation between lt IMT and Lt baPWV (r=0.527, p=0.006) were also recognized. Negative correlation between FMD and lt baPWV(r=-0.417, p=0.020) were observed, but there was no correlation between FMD and rt baPWV (r=-0.343, p=0.059).
Table 5 shows Spearman�s rank correlation coefficients for FMD, BAD, P-NTGD, NMD and FMD/NMD ratio with clinical and biochemical parameters in participants.. 
There was significantly positive correlation between FMD and eGFR (r= 0.348, p=0.041; Figure 1) and positive correlation between FMD/NMD ratio and eGFR (r=0.471, p=0.004; Figure 2). Negative correlation between P-NTGD and eGFR (r=-0.405, p=0.016; Figure 3) was recognized. There was weak negative correlation between FMD and SUA (r=-0.340, p=0.045).
Table 6 shows Spearman�s rank correlation for carotid IMT, baPWV and ankle brachial pressure index (ABI) with clinical and biochemical parameters in participants. 
Negative correlation between eGFR and rt IMT (r=-0.509, p=0.009) was detected, but here was no correlation between eGFR and lt IMT (r=-0.229, p=0.271). Correlation between eGFR and rt baPWV and lt baPWV were not shown. Positive correlation between SUA and rt IMT (r=0.613, p=0.001) and positive correlation between SUA and lt IMT (r=0.638, p=0.001) were also recognized. 
Table 7 shows correlation between SUA and other parameters in participant. There was weak negative correlation between SUA and eGFR (r=-0.335, p=0.049). 
We think that it was important to determine whether endothelial function was independent of the demographic variables. Multivariate regression analysis was not performed because of our small sample size.


Discussion
Patients with severe CKD have high risk of occurring CVD [2], but it has been reported that individuals with mild kidney dysfunction have also an increased CV risk in the community-based study [3]. It is reported that the increased risk of CVD has been attributed not only to cluster of CV risk factors [4] but also to endothelial dysfunction [5,6] in subjects with CKD. Though the threshold eGFR at which CV risk increases is not clear, expert consensus have proposed a level of < 60ml/min/1.73m2 [7], namely, the National Kidney Foundation clinical practice guidelines define CKD as the presence of eGFR less than 60 ml/min/1.73m2 with or without kidney damage for at least 3 months [7]. Previous studies have suggested that eGFR is associated with endothelial dysfunction in community-based [6, 8-11]. With regard to the restricting analysis to subject with eGFR>60ml/min/1.73m2, a few reports has been reported [9-11]. The Hoorn Study indicated that the inverse correlation between eGFR and biomarkers of endothelial function, namely plasma von Willebrand factor (VWF), soluble vascular cell adhesion molecule-1 (VCAM-1) and the urinary albumin-creatinine ratio in subjects unselected for CKD in a population-based cohort [6]. The Framingham Heart Study indicated that endothelial dysfunction estimated with FMD is not a major correlate of moderate CKD in subjects with stage 3 CKD, suggesting the focus on other mechanism such as inflammation and arterial stiffness [8].The Multi-Ethnic Study of Atherosclerosis (MESA) showed no association FMD with renal function in subjects with eGFR>60ml/min/1.73m2 [10]. Nerpin et al. reported that eGFR is associated with endothelial function in subjects with normal kidney function, but that this association is mainly explained by confounding CV risk factors [11].However, Study of Health in Pomerania (SHIP) indicated that FMD was associated with renal dysfunction in females with eGFR>60ml/min/1.73m2 [9]. They suggest that very mild renal dysfunction is considered as a risk factor for the early atherosclerosis disease process in women [9]. Our data showed that mild renal dysfunction assessed by eGFR value is respectively associated with endothelial function evaluated with FMD, FMD/NMD ratio which represents more sensitive than FMD [32] and P-NTGD. Meanwhile, P-NTGD value [33] which is without vascular tone and shows more stable marker than BAD [34]. BAD is the plausible surrogate marker of FMD. Our results showed the correlation between mild renal dysfunction and endothelial function. This indicates the possibility that mild renal dysfunction sensitively reflects endothelial function in women in cross-sectional study. 
The cardio-renal interrelationship by fine-turning by neurohumoral activity, namely atrial natriuretic peptide (ANP), renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS) has been reported under normal conditions [14]. It has been suggested that the interaction between the heart and the kidney may occur in the setting of processes and diseases such as advanced age, hypertension, diabetes mellitus and atherosclerosis [14]. Our result indicated that the cardio-renal relation may be also observed through endothelial dysfunction under mild renal dysfunction. It has been reported that endothelial dysfunction is considered as one of the pathophysiological major mechanism contributing to the relation of CVD and CKD [6,13,14]. Shang et al. reported microRNA-92a as a crucial link between CVD and CVD by mediated uremia-impaired endothelial dysfunction [35]. In addition to classic CVD risk factors, we suggest that mild renal dysfunction with eGFR>60ml/min/1.73m2 may be considered as CVD risk factors in female. 
Except the correlation between endothelial dysfunction and eGFR, Sonoda et al. reported the serum uric acid (SUA) as an independent predictor of future development of CKD in subject with eGFR>60ml/min/1.73m2 [15]. It has been also suggested that UA was independently related to the eGFR in the subject with eGFR>60ml/min/1.73m2 [16]. Meanwhile, experimental study indicated that hyperuricemia cause systemic and glomerular hypertension, leading to endothelial dysfunction and experimental hyperuricemia also contribute to an afferent renal arteriopathy and tubulointerstitial fibrosis in the kidney by activating the RAAS [17-20]. It is plausible that elevated SUA may contribute to endothelial dysfunction, inflammation, oxidative stress and renin-angiotensin system (RAS) activation [17] and leading to systemic atherosclerosis and/or reduced eGFR, namely, initiation and progression of CKD. As our data showed the weak inverse relationship between SUA and eGFR, the increased SUA level, even in physiological range, may be a risk factor for impaired eGFR in subjects with mild renal dysfunction. In other word, the raised SUA concentration, in physiological range, may reflect subclinical renal dysfunction.
The evidence of SUA to stimulate oxidant production has already been studied in both adipocytes [21] and VSMC [22 ].In addition to these studies, Yu et al. [23] have reported that SUA can induce oxidative stress and activation of local RAS system leading to senescence and apoptosis, showing a mechanism of uric acid-induced human umbilical vein endothelial dysfunction. Clinical studies have also indicated the relationship between SUA and endothelial dysfunction [24-27]. Our data showed a weak inverse correlation between SUA and endothelial function, suggesting the raised SUA, even in physiological range, reflect the possibility of the endothelial dysfunction. Even though, many CVD risk factors contribute to not only decreased FMD but also to impaired eGFR, we have focused on the SUA level which have the pleiotropic effects. We speculated that SUA may contribute to both decreased FMD and impaired eGFR.
 Well, Kanbay et al. have reported that allopurinol lowering SUA showed decreased SUA level, increased FMD value and increased eGFR level [26]. Our result may also indicate the interrelationship among SUA, endothelial dysfunction and eGFR, showing the linkage among these parameters. We speculate that the interactions among SUA, endothelial dysfunction and eGFR subsequently lead to systemic and/or renal atherosclerosis. 
Meanwhile, atherosclerosis and arteriosclerosis which are different vascular pathologies are present in CKD [13]. It has reported that progressive deteriolation of renal function in CKD is related with the uremic toxins, oxidative stress and inflammation, and develop the initiation of endothelial dysfunction and progression of atherosclerosis [13]. Endothelial dysfunction also cause arteriosclerosis, a dsease affecting the media of large and middle sized arteries with an increased collagen:elastin ratio, calcification and hyperplasia and hypertrophy of VSMCs, leading to the occurrence of increased arterial stiffness measured by PWV [13]. On the other hand, IMT is a marker which reflects not only early atherosclerosis, but also non-atherosclerotic compensatory remodeling with largely medial hypertrophy [28].In addition to the endothelial function assessed by brachial artery measures, we add the study whether eGFR.>60ml/min/1.73m2 value is correlated with these indicators. Negative correlation between eGFR and rt IMT was detected, but here was no correlation between eGFR and lt IMT. Correlation between eGFR and baPWV was not shown. 
Now, as FMD, IMT and baPWV examinations were measured by using different artery tree at different sites, a strong correlation between FMD and IMT were observed. Though IMT is strongly correlated with SUA, it has been reported that the region on chromosome 6 marked by rs4712972, including the SLC17A4, SLC17A1, and SLC17A3 genes demonstrated suggestive evidence for association with common IMT [35]. Recent genome-wide-association studies also have implicated this region with SUA [36]. A strong correlation between IMT value and SUA level in this study may reflect the genetic evidence.
Our results showed that correlation between mild renal dysfunction and endothelial function in the restricting study to subject with >60ml/min/1.73m2 was shown in women in cross-sectional study. This study indicate that the cardio-renal relationship was observed under mild renal dysfunction. In addition to classic CVD risk factors, we suggest that mild renal dysfunction in women with eGFR>60ml/min/1.73m2 may be considered as CVD risk factors. We suggest that the raised SUA level, even in physiological range, may reflect endothelial function and/or mild renal dysfunction. Our result also indicate interrelationship among SUA, endothelial dysfunction and eGFR. In other words, linking among SUA, endothelial function and eGFR may be putative, subsequently leading to systemic and/or renal atherosclerosis. 
Conclusions
Mild renal dysfunction may be associated with endothelial dysfunction, especially in women. The cardio-renal interrelationship may be also suggested under mild renal dysfunction. In addition to the traditional cardiovascular disease risk factors, we will indicate that mild renal dysfunction may be regarded as a cardiovascular disease risk factor in women. 

Compliance with ethical standards 
Informed consent was obtained from patients and healthy controls in this study and the study was approved by the Ethics Committee of NIihon University School of Medicine. 

Conflict of interest
Authors declare that they have no conflicts of interest.
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Figure legends
Figure 1 Positive correlation between FMD and eGFR was significantly observed. 

Figure 2 Significant positive correlation between FMD/NMD ratio and eGFR was shown.

 Figure 3 Significant negative correlation between P-NTGD and eGFR was observed.

Table 1. The Clinical and Biochemical Characteristics of the Participant (mean�SD)
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Variable 							Value (n=36) 
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Age years            					55.4�14.4  	
Heart rate beats/min    				69.7�11.1    	
SBP mmHg              				135.7�24.4  	
DBP mmHg            				80.3�15.5   	
Weight kg                 			55.2�9.7  
BMI kg/m2                				22.9�3.8
TC mg/dL                				211.2�39.9  	
TG mg/dL                				99.8�54.6  	
HDL-C mg/dL             				65.1�19.1
LDL-C mg/dL            				125.2�39.1
TC/HDL-C               				3.5�1.0
LDL/HDL               				2.1�0.8
Non-HDL-C mg/dL      				145.1�42.3
TG/HDL-C               				1.8�1.4
Glucose                 				94.7�8.5
HbA1c (NGSP)%         				5.3�0.3
UA mg/dL             				4.3�1.1
BUN mg/dL            				12.9�3.8
Cre mg/dL       			   	0.6�0.1  
eGFR ml/min/1.73m2   				83.7�12.1
Urine alb mg/day     					28.2�49.4
Renin pg/mL            				8.3�9.0
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Table 2. Brachial Artery Measures (mean�SD)  
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			Value (n=36) 		
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BAD-base mm    			 3.47�0.58    		  
BAD-max mm    			 3.67�0.56
FMD mm  			 0.20�0.11
FMD %            			 6.12�3.94    		
NMD %       			19.59�8.54 		     
P-NTGD mm      			 4.18�0.52 
FMD/NMD   			 0.36�0.23    		       		
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BAD: brachial artery diameter, BAD-base: BAD baseline diameter, BAD-max: BAD maximal diameter, FMD: flow-mediated vasodilation, NMD: nitroglycerin-mediated vasodilation, P-NTGD: post nitroglycerin brachial artery diameter 

Table 3. Spearman�s rank correlation coefficients of the brachial artery measures in participant with eGFR>60 ml/min/1.73m2
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	BAD-b 	BAD-m 	P-NTGD 	FMDmm 	FMD% 	NMD% 	FMD/NMD
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BAD-b            		0.97*    	0.90*    	-0.22   	-0.42  		-0.45    	0.001
BAD-m   	0.97*          		0.88*0		-0.06  		-0.27   	-0.42    	0.10
P-NTGD  	0.90*  		0.88*  0000		-0.19			-0.37   	-0.24  		-0.17
FMD mm 	-0.22 		-0.06   	-0.19      				0.96*   	0.11     	0.74*
FMD%    	-0.42  		-0.27   	-0.37   	0.96*            	0.21			0.68*
NMD %   	-0.45  		-0.42    	-0 24   	0.11    	0.21              	-0.46
FMD/NMD 	0.001  		0.10    	-0.17  		0.74*   	0.68*   	-0.46  	
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p <0.001


Table 4. Spearman s rank correlation coefficients of the atherosclerotic parameters in participant with eGFR.60ml/min/1.73m2       
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						FMD 		NMD 		FMD/NMD 	rtIMT 	ltIMT	rtPWV 	ltPWV
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FMD  0000  			0.21    	0.68*     		-0.66*  	-0.55 	-0.34  	-0.42
NMD    		0.21           		-0.46*    		-0.17  	-0.17 	-0.17   	-0.50
FMD/NMD 	0.68* 		-0.46*             		-0.390	-0.27 	-0.05   	-0.06            
rtIMT    		-0.66* 	-0.17   	-0.39               		0.64  	0.43    	0.48
ltIMT   			-0.55   	-0.17   	-0.27       	0.64           	0.50    	0.53  
rtPWV  			-0.34  	-0.17  	-0.05     		0.43    	0.50         		0.97*
ltPWV  			-0.42   	-0.50   	-0.060   		0.480		0.53  	0.97*   	
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p <0.001

Table 5. Spearman s rank correlation coefficients for FMD, BAD, P-NTGD, NMD and FMD/NMD with clinical and biochemical parameters in participants with eGFR>60ml/min/1.73m2       
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Age years           	-0.56* 	0.39*  	0.30    		-0.43* 	-0.19
TC mg/dl            	-0.23   	0.43*  	0.2600 	-0.55*  	0.19
TG mg/dl            	0.10   	0.10 	-0.003	  -0.52*  	0.33
HDL-C mg/dl        	-0.22  	-0.15  	-0.28     	0.17  		-0.19
TC/HDL-C           	0.08   	0.27   	0.27    		-0.41* 	0.28
LDL/HDL            	0.003 	0.33  	0.32    		-0.37* 	0.23
LDL-C mg/dl        	-0.10  	0.36*  	0.25  0		-0.47*  	0.24            
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TG/HDL-C          	0.14    	0.13   	0.12    		-0.42* 	0.28 
Glucose mg/dl       		-0.28   	0.33  	0.25    		-0.45*  	0.06
HbA1C (NGSP) %   		-0.18   	0.44*  	0.39*     	-0.47* 	0.20
Weight kg           	-0.02   	0.46*  	0.48*    	-0.41* 	0.28
BMI kg/m2          	-0.08  	0.32  	0.34     	-0.46* 	0.30
Waist cm           		-0.04  	0.42*  	0.42*    	-0.41*  	0.32
UA mg/dL         		 -0.34* 	0.11 	-0.07     	-0.03  	-0.22
SBP mmHg        		-0.14  	0.22 	0.14   		-0.43*  	0.09
DBP mmHg            	0.07   	0.05    0.06      	-0.12  	0.10
HR bpm            		-0.17  	0.05    	0.05    		-0.12  	-0.08
BUN mg/dl         		-0.05   	0.23   	0.19    		-0.21   	-0.19
Cre mg/dl           	-0.01   	0.01   	0.21     	0.42*  	-0.38*
eGFR ml/min/1.73m2  	0.35* 		-0.24  	-0.41*   	-0.18  	0.47*
Urine alb mg/day        0.08    -0.04  	-0.10      -0.26   	0.25
Renin pg/mL           	-0.09   	0.01   	-0.11      -0.14  	0.06
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p <0.05

Table 6. Spearman s rank correlation coefficients for IMT, baPWV and ABI with clinical and biochemical parameters in participant with eGFR>60ml/min/1.73m2 
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	IMT (R) 	IMT (L) 	PWV � 	PWV (L) 	ABI � 	ABI (L)
?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�?�
Age years          	0.58*   	0.45*   	0.68*   	0.76*    	0.40*   	0.28
TC mg/dl          	0.34   	0.50*0	0.39*  	0.40*    	0.34    	0.15
TG mg/dl          	0.18   	0.01   	0.43*  	0.40*    	0.05   	-0.08
HDL-C mg/dl      	-0.13   	0.06  		-0.18  	-0.13    		-0.003  	0.14
LDL-C mg/dl       	0.30   	0.35  		0.41*  	0.42*    	0.12  		-0.03
Non-HDL-C mg/dl 	0.33    	0.44*  	0.45*   	0.48*    	0.13   	-0.03              
Glucose mg/dl      	0.62*   	0.57*  	0.57*  	0.57*    	0.15    	0.04 
HbA1C (NGSP) % 	0.27    	0.31   	0.32   	0.34    		0.30   	0.02 
Weight kg         	0.24    	0.20   	0.07   	0.03    		0.07  		-0.07 
BMI kg/m2              	0.22    	0.30   	0.18   	0.18    		0.09    	-0.02 
Waist cm0000		0.49*0	0.25   	0.24   	0.22    		0.05  		-0.08
UA mg/dL       0 	0.61*  	0.64*   	0.06   	0.09    		-0.32   	-0.12
SBP mmHg        	0.46*  	0.47*  	0.67*  	0.60*   		-0.06   	-0.20
DBP mmHg        	0.37    	0.51*  	0.31    	0.22    		-0.08   	-0.21
HR bpm           	0.07   	0.17   	0.18   	0.17    		0.02   	-0.04  
BUN mg/dl        	0.16    	0.34   	0.22   	0.17     	0.12  		-0.09
Cre mg/dl          	0.29   	0.002 		-0.18  	-0.18    		0.05   	0.17 
eGFR ml/min/1.73m2 -0.51* 	-0.23   	-0.14    	-0.18    		-0.25   	-0.26 
Urine alb mg/day  	0.42   	0.32    	0.23    	0.21     	-0.13  	-0.32* 
Renin pg/mL      	0.03    	0.18    	0.06    	0.06     	0.05   	0.16  
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Table 7. Correlation between serum uric acid and other parameters in the participant with eGFR>60ml/min/1.73m2
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Age years             		0.0721                 	0.680
Waist cm                	0.352*                 	0.048 
Weight kg               	0.263                  	0.133 
BMI kg/m2              	0.382*                	0.037
AST U/L                	0.385*                 	0.022   
ALT U/L                	0.448*                	0.007
BUN mg/dL             	0.016                 	0.942
Creatinine mg/dL        	0.330                	0.053
eGFR ml/min/1.73m2     	-0.335*               	0.049
FMD %  0            0	-0.34* 000000	0.045    
FMD/NMD             	-0.221                	0.202 
NMD %                  	-0.033                 	0.850
P-NTGD mm             	-0.066                	0.704
rtIMT mm                	0.613*                	0.001
ltIMT mm                	0.638*                	0.001
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                                  Increased NMD in migraineurs




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