1. bookVolume 12 (2018): Edizione 6 (December 2018)
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Open Access

Elevation of serum adiponectin in mildly decreased glomerular filtration rate

Pubblicato online: 24 Oct 2019
Volume & Edizione: Volume 12 (2018) - Edizione 6 (December 2018)
Pagine: 255 - 262
Dettagli della rivista
License
Formato
Rivista
eISSN
1875-855X
Prima pubblicazione
01 Jun 2007
Frequenza di pubblicazione
6 volte all'anno
Lingue
Inglese

Adiponectin, also referred to as GBP28, apM1, AdipoQ, and Acrp30, is a 30-kDa polypeptide secreted exclusively by adipocyte that has functions in the regulation of glucose and lipid metabolisms [1]. Previous studies revealed the roles of adiponectin as an anti-inflammatory, anti-diabetic, and vascular protective adipokine [2, 3]. Reduction of serum adiponectin is associated with obesity [4, 5, 6], insulin resistance [7, 8], and cardiovascular diseases [9, 10]. In addition, serum adiponectin is described as an independent (inverse) risk of cardiovascular events and mortality among individuals with end-stage kidney disease [11]. Inversely, reports have shown that serum adiponectin increases in chronic kidney disease (CKD) [12, 13, 14], especially in individuals with end-stage kidney disease [15]. When the kidney is damaged or impaired, the glomerular filtration rate (GFR) decreases, resulting in an accumulation of adiponectin in blood circulation [11].

CKD is a noncommunicable disease, which is the global epidemic with increasing prevalence [16]. CKD is defined as abnormalities of kidney structure or function for >3 months [17], which may be detected by decreases in GFR and/or the presence of proteinuria. As a result, CKD individuals are classified into five stages; stage 1, normal GFR (eGFR ≥ 90 mL/min/1.73 m2); stage 2, mild kidney damage (eGFR = 60–89 mL/min/1.73 m2); stage 3, moderate kidney damage (eGFR = 30–59 mL/min/1.73 m2); stage 4, severe kidney damage (eGFR = 15–29 mL/min/1.73 m2); and stage 5, kidney failure (eGFR < 15 mL/min/ 1.73 m2); Moderate-to-severe kidney damage (eGFR < 60 mL/min/1.73 m2) is associated with albuminuria [18, 19]. The albuminuria categories in CKD are stratified according to urinary albumin excretion (UAE; mg/24 h) and urine albumin-to-creatinine ratio (UACR; mg/g) <30, 30–300, or >300, which fits well with the classification of normal to mildly increased, moderately, and severely increased albuminuria, respectively [20]. Stages 1 and 2 are described as the early stage of CKD and usually have no signs and symptoms. However, it can be diagnosed by slightly elevated serum creatinine and the presence of normal to mildly increased albuminuria, caused by a decline in glomerular and tubular functions [21].

As serum adiponectin markedly increases in end-stage kidney disease, it may reflect in the early stage of CKD. Therefore, this study aimed to assess levels of serum adiponectin in mildly decreased GFR, examine the relationship between serum adiponectin and other parameters, and evaluate serum adiponectin as the risk factor of mildly decreased GFR.

Materials and methods
Study population

This cross-sectional study included 172 volunteers (36 males and 136 females) at the age of 35–60 years with no history of type 1 and type 2 diabetes, cardiovascular disease, CKD with eGFR <60 mL/min/1.73 m2, UACR > 300 mg/g, use of drugs that affect kidney and liver functions, such as analgesic, antipyretic, and antibiotic drugs. Based on estimated glomerular filtration rate (eGFR) defined by the Kidney Disease: Improving Global Outcomes (KDIGO: 2012) [22], they were classified into two groups: 82 cases with mildly decreased eGFR (G2, eGFR = 60–89 mL/min/1.73m2) and 90 with normal eGFR (G1, eGFR ≥ 90 mL/min/1.739m2). Anthropometric data (gender, age, weight, blood pressure, and waist and hip circumferences) were collected. This study protocol was approved by the Human Research Ethics Committee at Thammasat University (certificate of approval No. 119/2559) and informed consent was obtained from all participants.

Sample collection and biochemical analysis

Overnight (8–12 h) fasting blood and urine were collected and placed immediately on ice. Plasma and serum samples were prepared by centrifugation at 1000× g for 5–10 min and kept at –70ºC until further analysis. Fasting plasma glucose (FPG), total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-cholesterol), low-density lipoprotein cholesterol (LDL-cholesterol) and creatinine were measured using the automated blood analyzer (Dxc800; Beckman Coulter). Calculation of eGFR was done using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation, 2012 [23, 24]. Urine albumin was measured by the immunoturbidimetric assay (manufacturer). UACR was calculated using urine albumin in milligram (mg) and urine creatinine in gram (g). Serum adiponectin was analyzed using the sandwich enzyme-linked immunosorbent assay kit (DY1065, R&D system), which was verified. The percent recovery was 97.36% and the inter-assay and intra-assay coefficients of variation were 6.93% and 7.31%, respectively.

Statistical analyses

Data were reported as means ± standard deviation (SD) and analyzed using SPSS software version 23; IBM USA. Data comparisons for continuous variables between two groups were performed using the Mann–Whiney U test. The Kruskal– Wallis tests were used to analyze the statistical difference between the three groups (P < 0.05). When significance was observed, a post-hoc test was used for pairwise analyses (P < 0.05). Spearman’s rank correlation coefficients were used to examine the correlation between serum adiponectin and other parameters. Multiple linear regression analysis was used to evaluate the effects of other confounding factors for serum adiponectin. Univariate and multivariate analyses were conducted using a logistic regression with 95% confidence interval. P < 0.05 was considered a statistical significance. Receiver operating characteristic (ROC) curve showed the plot between specificity and sensitivity of serum adiponectin levels at a cutoff point as a predictor for mildly decreased eGFR.

Results
Baseline characteristics

Anthropometric data and biochemical variables of individuals with normal (G1, control, n = 90) and mildly decreased eGFR (G2, n = 82) are shown in Table 1. Ages, blood pressure, serum creatinine, HDL-cholesterol, and serum adiponectin were significantly higher in the G2 group than the G1 control. Waist circumference, waist per hip ratio (WHR), body adiposity index (BAI), triglyceride, and UACR slightly increased in the G2 group; however, there was no significant difference between the G2 and G1 groups. Both G1 and G2 groups have similar weight, body mass index (BMI), FPG, total cholesterol, and LDL-cholesterol.

Anthropometric characteristics and biochemical variables of the mildly decreased eGFR (G2) and the normal eGFR (G1)

VariablesNormal eGFR (G1)Mildly decreased eGFR (G2)P
(n = 90)(n = 82)
Sex
Male, n (%)14 (16)22 (27)
Female, n (%)76 (84)60 (73)0.069a
Age (years)43.52 ± 5.9250.17 ± 6.42<0.001*b
Weight (kg)63.53 ± 12.3662.24 ± 9.990.760b
Body mass index (kg/m2)24.697 ± 3.8724.09 ± 3.100.624b
Waist (cm)82.56 ± 10.1483.72 ± 8.350.278b
Hip (cm)98.94 ± 8.9197.54 ± 7.500.331b
Waist-to-hip ratio0.84 ± 0.070.86 ± 0.060.062b
DBP (mmHg)75.89 ± 9.3380.20 ± 10.34<0.001*b
SBP (mmHg)116.28 ± 12.46124.32 ± 13.25<0.001*b
Body adipose30.98 ± 4.8830.20 ± 4.960.274b
Creatinine (mg/dL)0.70 ± 0.110.92 ± 0.14<0.001*b
eGFR105.02 ± 8.3380.20 ± 6.98<0.001*b
UACR (mg/g)6.71 ± 4.278.13 ± 9.390.582b
FPG (mg/dL)88.44 ± 6.5688.91 ± 6.970.630b
Cholesterol (mg/dL)225.56 ± 50.23229.27 ± 45.450.480b
Triglyceride (mg/dL)113.42 ± 54.58125.43 ± 69.300.321b
HDL-C (mg/dL)54.29 ± 14.5460.61 ± 15.160.012*b
LDL-C (mg/dL)144.36 ± 38.66143.45 ± 40.130.800b
Serum adiponectin (mg/mL)6.57 ± 3.248.23 ± 3.26<0.001*b

DBP, diastolic blood pressure; SBP, systolic blood pressure; eGFR, estimated glomerular filtration rate; UACR, urine albumin-to-creatinine ratio; FPG, Fasting plasma glucose; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol.

Categorical variables are shown as percentage (%).

aChi-square test

bMann–Whitney U test

*P < 0.05 was considered significant.

Serum adiponectin in mildly decreased eGFR

Serum adiponectin was higher in individuals with mildly decreased eGFR (G2, 8.23 ± 3.26 mg/mL) than in the G1 control (6.57 ± 3.24 mg/mL) with the P value of 0.001 (Figure 1). In the G2 group, females had higher serum adiponectin than males (8.92 ± 3.41 and 6.28 ± 1.76 mg/mL, respectively) with the P value of 0.002. However, the G1 control showed no significant differences in serum adiponectin between males and females (5.39 ± 2.99 and 6.79 ± 3.26 mg/mL, respectively) with the P values of 0.101 (Figure 2).

Figure 1

Comparison of the serum adiponectin between the mildly decreased eGFR (G2) and the control with normal eGFR (G1). P: Mann–Whiney U test

Figure 2

Comparison of serum adiponectin in male (open bars) and female (solid bars) in the mildly decreased eGFR (G2) and the control with normal eGFR (G1). P: Mann–Whiney U test

When data were classified based on Asian BMI criteria [25] as normal weight (18.5–22.9 kg/m2), overweight (23.0– 24.9 kg/m2), and obesity (≥25.0 kg/m2), it was shown that serum adiponectin in each group was higher in the G2 than the G1 control. However, the significant difference (P < 0.05) was found only in G1 control. Serum adiponectin levels were significantly lower in the obesity than the overweight and the normal weight with P value of 0.025 and 0.034, respectively (Figure 3).

Figure 3

Comparison of serum adiponectin between the normal eGFR (gray bar) and the mildly decreased eGFR (black bar) among normal weight, overweight, and obesity based on Asian BMI. The Kruskal–Wallis test followed by a post-hoc test was used to determine the differences between three independent groups and all pairwise comparisons. (*P < 0.05 vs normal weight group and obese group and overweight group and obese group)

The Spearman’s rank correlation coefficient test revealed the correlations between serum adiponectin and anthropometric parameters and biochemical variables (Table 2). Serum adiponectin was significantly correlated with ages (r = 0.355), gender (r = 0.196), weight (r = –0.306), BMI (r = –0.217), waist circumference (r = –0.236), hip circumference (r = –0.256), eGFR (r = –0.257), triglyceride (r = –0.204), and HDL-cholesterol (r = 0.444), but not significantly correlated with WHR, BAI, creatinine, UACR, FPG, total cholesterol, LDL-cholesterol, and blood pressure. Multiple linear regression analysis setting serum adiponectin as a dependent factor showed that ages, HDL-cholesterol, and LDL-cholesterol were independently and significantly associated with serum adiponectin (Table 3).

Bivariate spearman’s rank correlation coefficients between serum adiponectin with anthropometric characteristics and biochemical variables

VariablesSerum adiponectin (µg/mL)
rP
Age (year)0.355<0.001*
Weight (kg)-0.306<0.001*
Body mass index (kg/m2)-0.2170.004*
Waist (cm)-0.2360.002*
Hip (cm)-0.2560.001*
Waist-to-hip ratio-0.1050.168
DBP (mmHg)-0.0710.358
SBP (mmHg)0.0040.963
Body adiposity index-0.0680.379
Creatinine (mg/dL)-0.0730.344
eGFR-0.2570.001*
UACR (mg/g)0.1080.159
FPG (mg/dL)-0.0050.947
Cholesterol (mg/dL)-0.0560.469
Triglyceride (mg/dL)-0.2040.007*
HDL-C (mg/dL)0.444<0.001*
LDL-C (mg/dL)-0.0820.283

Spearman’s rank correlation coefficients, *P < 0.05 was considered significant.

Multiple linear regression with adiponectin as a dependent variable (N = 172)

Independent variablesUnstandardized coefficientsStandardized coefficientstP < 0.05
BStd. ErrorBeta
Constant22.19036.0210.6160.539
Age (year)0.1170.0520.2442.2480.026*
Weight (kg)0.2440.2470.8220.9890.324
BMI (kg/m2)–0.5950.643–0.627–0.9260.356
Waist (cm)–0.0780.264–0.216–0.2950.769
Hip (cm)–0.0940.343–0.233–0.2750.784
Waist-to-hip ratio3.97624.3280.0840.1630.870
DBP (mmHg)–0.0500.032–0.150–1.5340.127
SBP (mmHg)0.0190.0250.0770.7830.435
Body adiposity index0.1820.4850.2680.3750.708
Creatinine (mg/dL)–1.4514.985–0.073–0.2910.771
eGFR–0.0300.053–0.129–0.5620.575
UACR (mg/g)0.0210.0310.0450.6640.508
FPG (mg/dL)0.0540.0350.1081.5540.122
Cholesterol (mg/dL)0.0200.0110.2891.9090.058
Triglyceride (mg/dL)–0.0060.005–0.103–1.1520.251
HDL-C (mg/dL)0.0530.0200.2412.6510.009*
LDL-C (mg/dL)–0.0300.012–0.351–2.5370.012*
Constant = 22.190; R = 0.600; R2 = 0.280; SEest= ±2.82; F = 4.494; P <0.05

Serum adiponectin = 22.190 + 0.117 (Age) +0.053 (HDL-C) -0.030 (LDL-C).

The univariate and multivariate logistic regression analyses for a predictive index of mildly decreased eGFR are summarized in Table 4. Univariate regression showed that individuals older than 46 years, hypertension (systolic blood pressure [SBP] ≥130 mmHg, diastolic blood pressure [DBP] ≥ 85 mmHg), and serum adiponectin (cutoff = 5.7 mg/mL) were significantly associated with the mildly decreased eGFR (G2). Multivariate regression analysis showed that individuals at the ages of 46–55 years (4.0; 95% CI: 1.9–8.3) and >55 years (11.4; 95% CI: 3.7–33.5) were significantly correlated with the mildly decreased eGFR after adjusting for age, SBP, DBP, and serum adiponectin (Table 4). ROC curve analysis of serum adiponectin for detection of mildly decreased eGFR (G2) showed 70.7% specificity and 50% sensitivity at the cutoff value of 5.70 mg/mL. The area under the ROC curve was 0.652 (95% CI: 0.570–0.733, P = 0.001).

Univariate and multivariate analyses of risk for mildly decreased eGFR

VariablesCaseControlCrude ORPAdjusted ORP
N (%)N (%)(95%Cl)(95%Cl)
Sex
Male22 (26.8)14 (15.6)1
Female60 (73.2)76 (84.4)0.5 (0.2–1.1)0.072
Age (years)
35–4520 (24.4)60 (66.7)11
46–5538 (46.3)25 (27.8)4.5 (2.2–9.3)<0.001*4.0 (1.9–8.3)<0.001*
>5524 (29.3)5 (5.5)14.4 (4.9–42.8)<0.001*11.4 (3.7–35.5)<0.001*
Body mass index (kg/m2)
Normal30 (36.6)30 (33.3)1
Overweight27 (37.9)30 (33.3)0.9 (0.4–1.9)0.776
Obese25 (30.5)30 (33.3)0.8 (0.4–1.7)0.626
Waist-to-hip ratio
Male ≤0.90, Female ≤0.8552 (63.4)63 (70.0)1
Male >0.90, Female >0.8530 (36.6)27 (30.0)1.3 (0.7–2.5)0.360
SBP (mmHg)
<13057 (69.5)77 (85.6)11
≥13025 (30.5)13 (14.4)2.6 (1.2–5.5)0.013*1.2 (0.4–3.4)0.689
DBP (mmHg)
<8553 (64.6)75 (83.3)11
≥8529 (35.4)15 (16.7)2.7 (1.4–5.9)0.006*2.2 (0.8–5.5)0.112
Glucose (mg/dL)
<10078 (95.1)89 (5.6)1
≥1004 (4.9)1 (1.1)4.5 (0.5–41.7)0.179
Cholesterol (mg/dL)
<20018 (22.0)28 (31.1)1
≥20064 (78.0)62 (68.9)1.6 (0.8–3.2)0.177
Triglyceride (mg/dL)
<15058 (70.7)71 (78.9)1
≥15024 (29.3)19 (21.1)1.5 (0.8–3.1)0.219
HDL-C (mg/dL)
Male ≥40, Female ≥5014 (17.1)23 (25.6)1
Male <40, Female <5068.6 (82.9)67 (74.4)1.6 (0.8–3.5)0.179
LDL-C (mg/dL)
<10011 (12.6)9 (10.0)1
≥10076 (87.4)81 (90.0)0.8 (0.3–2.1)0.647
Serum adiponectin (mg/mL)
<5.7024 (29.3)45 (50.0)11
≥5.7058 (70.7)45 (50.0)2.4 (1.3–4.5)0.006*1.7 (0.8–3.5)0.147

OR, odd ratio; CI, confidence interval; DBP, diastolic blood pressure; SBP, systolic blood pressure; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol.

*P < 0.05 was considered significant.

Discussion

The present study revealed, for the first time, that serum adiponectin increased in individuals with mildly decreased eGFR (G2) compared to normal (G1) in all groups; normal weight, overweight, and obesity. This was consistent with previous studies showing that serum adiponectin levels increase in CKD patients [12, 13, 14]. The possible explanation was that inflammatory stimuli found in CKD induce adiponectin expression in renal tubular cells to trigger a feedback response [26], leading to increases in circulating adiponectin levels.

Adiponectin was significantly higher in normal glucose tolerance group than in impaired fasting glucose and type 2 diabetes mellitus groups [27]. Diabetes mellitus was an exclusion criterion in our study. Even though, 5% of total volunteers (9/172 persons) were presented with impair glucose tolerance (IGT) state. There were four persons in the G1 group and five persons in the G2 group with FPG values of 100–107 mg/dL (The cutoff for IGT was defined as FPG = 100−125 mg/dL, according to current American Diabetes Association (ADA) criteria [28]). Similar results as shown in Table 1 were found after nine persons with IGT were excluded. Serum adiponectin was still higher in the mildly decreased eGFR group (7.35 ± 3.35 µg/mL) than the normal eGFR group (6.54 ± 3.19 µg/mL) with statistical significance at P < 0.05.

Previous reports have shown that obese individuals have lower serum adiponectin than normal weight [29, 30]. Similarly, our study showed that serum adiponectin levels were lower in obesity than normal weight individuals. In addition, low levels of serum adiponectin increase risks of CKD in the obese [3]. Obesity causes marked structural changes in kidneys, leading to loss of nephron function, increases in arterial pressure, and severe renal injury [31]. Furthermore, we observed that serum adiponectin was higher in females than males. Similar findings were shown by Eglit et al. [32], Cnop et al. [33], and Nishizawa et al. [34] that serum adiponectin concentrations were higher in females than in males. This can be explained that males have higher testosterone levels and the hormone suppresses the secretion of adiponectin [33, 34].

Moreover, our results indicated that serum adiponectin levels were positively correlated with age, and HDL-cholesterol, but negatively correlated with weight, BMI, eGFR, triglyceride, and waist and hip circumferences (Table 2). These findings are consistent with the previous studies in healthy, obesity, type-2 diabetes, CKD, and end-stage kidney disease subjects, showing that serum adiponectin was negatively related with BMI, weight, triglyceride, eGFR, and waist and hip circumferences [12, 14, 35, 36] and positively related with age [37] and HDL-cholesterol [5, 38].

We also found that serum adiponectin depended on age, HDL-cholesterol, and LDL-cholesterol (Table 3). The univariate analysis found that serum adiponectin was correlated with mildly decreased eGFR (Table 4). However, after adjustment for gender, age, and blood pressure, the associations between serum adiponectin and mildly decreased eGFR did not reach statistical significance. Therefore, serum adiponectin was not considered an independent risk factor for mildly kidney damage. Multivariate regression analysis showed that only age was significantly correlated with the mildly decreased eGFR. Hypertension is defined by SBP ≥ 130 mmHg and/or DBP ≥ 85 mmHg, and the present study revealed that 30.5% and 35.4% of individuals with mildly kidney damage had SBP ≥ 130 mmHg and DBP ≥ 85 mmHg, respectively. Hypertension is not only a cause but also a consequence of CKD [39, 40]. Therefore, hypertension might be the main cause of mildly decreased eGFR in this study.

ROC curve analysis of serum adiponectin for classifying a mildly decreased eGFR from a normal eGFR showed 70.7% specificity and 50% sensitivity when using 5.70 µg/mL as a cutoff value. The area under the ROC curve was 0.652 (95% CI: 0.570–0.733, P = 0.001). It is known that serum adiponectin decreases in diseases, such as obesity, diabetes mellitus, and cardiovascular diseases [4, 5, 6, 7, 8, 9, 10]; however, increases in adiponectin in blood circulation are found in kidney damage or CKD. Therefore, it is possible that serum adiponectin levels can be useful as a follow-up biomarker to predict the CKD progression.

Conclusion

Serum adiponectin significantly increased in individuals with mildly decreased eGFR. These findings suggested that increases in serum adiponectin reflected the reduction of kidney functions. In addition, univariate and multivariate analyses implied that serum adiponectin may be a modulating factor, but is not an independent risk factor for mildly kidney damage.

Figure 1

Comparison of the serum adiponectin between the mildly decreased eGFR (G2) and the control with normal eGFR (G1). P: Mann–Whiney U test
Comparison of the serum adiponectin between the mildly decreased eGFR (G2) and the control with normal eGFR (G1). P: Mann–Whiney U test

Figure 2

Comparison of serum adiponectin in male (open bars) and female (solid bars) in the mildly decreased eGFR (G2) and the control with normal eGFR (G1). P: Mann–Whiney U test
Comparison of serum adiponectin in male (open bars) and female (solid bars) in the mildly decreased eGFR (G2) and the control with normal eGFR (G1). P: Mann–Whiney U test

Figure 3

Comparison of serum adiponectin between the normal eGFR (gray bar) and the mildly decreased eGFR (black bar) among normal weight, overweight, and obesity based on Asian BMI. The Kruskal–Wallis test followed by a post-hoc test was used to determine the differences between three independent groups and all pairwise comparisons. (*P < 0.05 vs normal weight group and obese group and overweight group and obese group)
Comparison of serum adiponectin between the normal eGFR (gray bar) and the mildly decreased eGFR (black bar) among normal weight, overweight, and obesity based on Asian BMI. The Kruskal–Wallis test followed by a post-hoc test was used to determine the differences between three independent groups and all pairwise comparisons. (*P < 0.05 vs normal weight group and obese group and overweight group and obese group)

Anthropometric characteristics and biochemical variables of the mildly decreased eGFR (G2) and the normal eGFR (G1)

VariablesNormal eGFR (G1)Mildly decreased eGFR (G2)P
(n = 90)(n = 82)
Sex
Male, n (%)14 (16)22 (27)
Female, n (%)76 (84)60 (73)0.069a
Age (years)43.52 ± 5.9250.17 ± 6.42<0.001*b
Weight (kg)63.53 ± 12.3662.24 ± 9.990.760b
Body mass index (kg/m2)24.697 ± 3.8724.09 ± 3.100.624b
Waist (cm)82.56 ± 10.1483.72 ± 8.350.278b
Hip (cm)98.94 ± 8.9197.54 ± 7.500.331b
Waist-to-hip ratio0.84 ± 0.070.86 ± 0.060.062b
DBP (mmHg)75.89 ± 9.3380.20 ± 10.34<0.001*b
SBP (mmHg)116.28 ± 12.46124.32 ± 13.25<0.001*b
Body adipose30.98 ± 4.8830.20 ± 4.960.274b
Creatinine (mg/dL)0.70 ± 0.110.92 ± 0.14<0.001*b
eGFR105.02 ± 8.3380.20 ± 6.98<0.001*b
UACR (mg/g)6.71 ± 4.278.13 ± 9.390.582b
FPG (mg/dL)88.44 ± 6.5688.91 ± 6.970.630b
Cholesterol (mg/dL)225.56 ± 50.23229.27 ± 45.450.480b
Triglyceride (mg/dL)113.42 ± 54.58125.43 ± 69.300.321b
HDL-C (mg/dL)54.29 ± 14.5460.61 ± 15.160.012*b
LDL-C (mg/dL)144.36 ± 38.66143.45 ± 40.130.800b
Serum adiponectin (mg/mL)6.57 ± 3.248.23 ± 3.26<0.001*b

Multiple linear regression with adiponectin as a dependent variable (N = 172)

Independent variablesUnstandardized coefficientsStandardized coefficientstP < 0.05
BStd. ErrorBeta
Constant22.19036.0210.6160.539
Age (year)0.1170.0520.2442.2480.026*
Weight (kg)0.2440.2470.8220.9890.324
BMI (kg/m2)–0.5950.643–0.627–0.9260.356
Waist (cm)–0.0780.264–0.216–0.2950.769
Hip (cm)–0.0940.343–0.233–0.2750.784
Waist-to-hip ratio3.97624.3280.0840.1630.870
DBP (mmHg)–0.0500.032–0.150–1.5340.127
SBP (mmHg)0.0190.0250.0770.7830.435
Body adiposity index0.1820.4850.2680.3750.708
Creatinine (mg/dL)–1.4514.985–0.073–0.2910.771
eGFR–0.0300.053–0.129–0.5620.575
UACR (mg/g)0.0210.0310.0450.6640.508
FPG (mg/dL)0.0540.0350.1081.5540.122
Cholesterol (mg/dL)0.0200.0110.2891.9090.058
Triglyceride (mg/dL)–0.0060.005–0.103–1.1520.251
HDL-C (mg/dL)0.0530.0200.2412.6510.009*
LDL-C (mg/dL)–0.0300.012–0.351–2.5370.012*
Constant = 22.190; R = 0.600; R2 = 0.280; SEest= ±2.82; F = 4.494; P <0.05

Univariate and multivariate analyses of risk for mildly decreased eGFR

VariablesCaseControlCrude ORPAdjusted ORP
N (%)N (%)(95%Cl)(95%Cl)
Sex
Male22 (26.8)14 (15.6)1
Female60 (73.2)76 (84.4)0.5 (0.2–1.1)0.072
Age (years)
35–4520 (24.4)60 (66.7)11
46–5538 (46.3)25 (27.8)4.5 (2.2–9.3)<0.001*4.0 (1.9–8.3)<0.001*
>5524 (29.3)5 (5.5)14.4 (4.9–42.8)<0.001*11.4 (3.7–35.5)<0.001*
Body mass index (kg/m2)
Normal30 (36.6)30 (33.3)1
Overweight27 (37.9)30 (33.3)0.9 (0.4–1.9)0.776
Obese25 (30.5)30 (33.3)0.8 (0.4–1.7)0.626
Waist-to-hip ratio
Male ≤0.90, Female ≤0.8552 (63.4)63 (70.0)1
Male >0.90, Female >0.8530 (36.6)27 (30.0)1.3 (0.7–2.5)0.360
SBP (mmHg)
<13057 (69.5)77 (85.6)11
≥13025 (30.5)13 (14.4)2.6 (1.2–5.5)0.013*1.2 (0.4–3.4)0.689
DBP (mmHg)
<8553 (64.6)75 (83.3)11
≥8529 (35.4)15 (16.7)2.7 (1.4–5.9)0.006*2.2 (0.8–5.5)0.112
Glucose (mg/dL)
<10078 (95.1)89 (5.6)1
≥1004 (4.9)1 (1.1)4.5 (0.5–41.7)0.179
Cholesterol (mg/dL)
<20018 (22.0)28 (31.1)1
≥20064 (78.0)62 (68.9)1.6 (0.8–3.2)0.177
Triglyceride (mg/dL)
<15058 (70.7)71 (78.9)1
≥15024 (29.3)19 (21.1)1.5 (0.8–3.1)0.219
HDL-C (mg/dL)
Male ≥40, Female ≥5014 (17.1)23 (25.6)1
Male <40, Female <5068.6 (82.9)67 (74.4)1.6 (0.8–3.5)0.179
LDL-C (mg/dL)
<10011 (12.6)9 (10.0)1
≥10076 (87.4)81 (90.0)0.8 (0.3–2.1)0.647
Serum adiponectin (mg/mL)
<5.7024 (29.3)45 (50.0)11
≥5.7058 (70.7)45 (50.0)2.4 (1.3–4.5)0.006*1.7 (0.8–3.5)0.147

Bivariate spearman’s rank correlation coefficients between serum adiponectin with anthropometric characteristics and biochemical variables

VariablesSerum adiponectin (µg/mL)
rP
Age (year)0.355<0.001*
Weight (kg)-0.306<0.001*
Body mass index (kg/m2)-0.2170.004*
Waist (cm)-0.2360.002*
Hip (cm)-0.2560.001*
Waist-to-hip ratio-0.1050.168
DBP (mmHg)-0.0710.358
SBP (mmHg)0.0040.963
Body adiposity index-0.0680.379
Creatinine (mg/dL)-0.0730.344
eGFR-0.2570.001*
UACR (mg/g)0.1080.159
FPG (mg/dL)-0.0050.947
Cholesterol (mg/dL)-0.0560.469
Triglyceride (mg/dL)-0.2040.007*
HDL-C (mg/dL)0.444<0.001*
LDL-C (mg/dL)-0.0820.283

Diez JJ, Iglesias P. The role of the novel adipocyte-derived hormone adiponectin in human disease. Eur J Endocrinol. 2003; 148:293–300.DiezJJIglesiasPThe role of the novel adipocyte-derived hormone adiponectin in human diseaseEur J Endocrinol200314829330010.1530/eje.0.148029312611609Search in Google Scholar

Kim HY, Bae EH, Ma SK, Chae DW, Choi KH, Kim Y-S, et al. Association of serum adiponectin level with albuminuria in chronic kidney disease patients. Clin Exp Nephrol. 2016; 20:443–9.KimHYBaeEHMaSKChaeDWChoiKHKimY-Set alAssociation of serum adiponectin level with albuminuria in chronic kidney disease patientsClin Exp Nephrol201620443910.1007/s10157-015-1173-426445954Search in Google Scholar

Sweiss N, Sharma K. Adiponectin effects on the kidney. Best Pract Res Clin Endocrinol Metab. 2014; 28:71–9.SweissNSharmaKAdiponectin effects on the kidneyBest Pract Res Clin Endocrinol Metab20142871910.1016/j.beem.2013.08.002425256724417947Search in Google Scholar

Tungtrongchitr R, Sricharoen P, Pongpaew P, Phonrat B, Arthan D, Vudhivai N, et al. Adiponectin/ACP30, a collagen-like plasma protein in relation to anthropometric measurement in Thai overweight and obese subjects. Int J Food Sci Nutr. 2005; 56:193–201.TungtrongchitrRSricharoenPPongpaewPPhonratBArthanDVudhivaiNet alAdiponectin/ACP30, a collagen-like plasma protein in relation to anthropometric measurement in Thai overweight and obese subjectsInt J Food Sci Nutr20055619320110.1080/0963748050015411316009634Search in Google Scholar

Yang WS, Lee WJ, Funahashi T, Tanaka S, Matsuzawa Y, Chao CL, et al. Plasma adiponectin levels in overweight and obese Asians. Obesity. 2002; 10:1104–10.YangWSLeeWJFunahashiTTanakaSMatsuzawaYChaoCLet alPlasma adiponectin levels in overweight and obese AsiansObesity20021011041010.1038/oby.2002.15012429873Search in Google Scholar

Nigro E, Scudiero O, Monaco ML, Palmieri A, Mazzarella G, Costagliola C, et al. New insight into adiponectin role in obesity and obesity-related diseases. Biomed Res Int. 2014; 2014:1–14.NigroEScudieroOMonacoMLPalmieriAMazzarellaGCostagliolaCet alNew insight into adiponectin role in obesity and obesity-related diseasesBiomed Res Int2014201411410.1155/2014/658913410942425110685Search in Google Scholar

Aleidi S, Issa A, Bustanji H, Khalil M, Bustanji Y. Adiponectin serum levels correlate with insulin resistance in type 2 diabetic patients. Saudi Pharm J. 2015; 23:250–6.AleidiSIssaABustanjiHKhalilMBustanjiYAdiponectin serum levels correlate with insulin resistance in type 2 diabetic patientsSaudi Pharm J201523250610.1016/j.jsps.2014.11.011447581326106273Search in Google Scholar

Blaslov K, Bulum T, Zibar K, Duvnjak L. Relationship between adiponectin level, insulin sensitivity, and metabolic syndrome in type 1 diabetic patients. Int J Endocrinol. 2013; 2013:1–6.BlaslovKBulumTZibarKDuvnjakLRelationship between adiponectin level, insulin sensitivity, and metabolic syndrome in type 1 diabetic patientsInt J Endocrinol201320131610.1155/2013/535906373022523956744Search in Google Scholar

Shibata R, Ouchi N, Murohara T. Adiponectin and cardiovascular disease. Circ J. 2009; 73:608–14.ShibataROuchiNMuroharaTAdiponectin and cardiovascular diseaseCirc J2009736081410.1253/circj.CJ-09-005719261992Search in Google Scholar

Siasos G, Tousoulis D, Kollia C, Oikonomou E, Siasou Z, Stefanadis C, et al. Adiponectin and cardiovascular disease: mechanisms and new therapeutic approaches. Curr Med Chem. 2012; 19:1193–209.SiasosGTousoulisDKolliaCOikonomouESiasouZStefanadisCet alAdiponectin and cardiovascular disease: mechanisms and new therapeutic approachesCurr Med Chem201219119320910.2174/09298671279932058322257055Search in Google Scholar

Menon V, Li L, Wang X, Greene T, Balakrishnan V, Madero M, et al. Adiponectin and mortality in patients with chronic kidney disease. J Am Soc Nephrol. 2006; 17:2599–606.MenonVLiLWangXGreeneTBalakrishnanVMaderoMet alAdiponectin and mortality in patients with chronic kidney diseaseJ Am Soc Nephrol200617259960610.1681/ASN.2006040331Search in Google Scholar

Kamimura MA, Canziani MEF, Sanches FR, Velludo CM, Carrero JJ, Bazanelli AP, et al. Variations in adiponectin levels in patients with chronic kidney disease: a prospective study of 12 months. J Bras Nefrol. 2012; 34:259–65.KamimuraMACanzianiMEFSanchesFRVelludoCMCarreroJJBazanelliAPet alVariations in adiponectin levels in patients with chronic kidney disease: a prospective study of 12 monthsJ Bras Nefrol2012342596510.5935/0101-2800.20120007Search in Google Scholar

Saginova E, Galliamov M, Severova M, Surkova O, Fomin V, Ermakov N, et al. The role of leptin, adiponectin and insulin-resistance markers in development of early stages of chronic kidney disease and atherosclerosis of carotid arteries in obese patients. Ter Arkh. 2011; 83:47–53.SaginovaEGalliamovMSeverovaMSurkovaOFominVErmakovNet alThe role of leptin, adiponectin and insulin-resistance markers in development of early stages of chronic kidney disease and atherosclerosis of carotid arteries in obese patientsTer Arkh2011834753Search in Google Scholar

Sedighi O, Abediankenari S. Relationship between plasma adiponectin level with inflammatory and metabolic markers in patients with chronic kidney disease. Nephrourol Mon. 2014; 6:1–4.SedighiOAbediankenariSRelationship between plasma adiponectin level with inflammatory and metabolic markers in patients with chronic kidney diseaseNephrourol Mon201461410.5812/numonthly.11743Search in Google Scholar

Shen YY, Charlesworth JA, Kelly JJ, Loi KW, Peake PW. Up-regulation of adiponectin, its isoforms and receptors in end-stage kidney disease. Nephrol Dial Transplant. 2006; 22:171–8.ShenYYCharlesworthJAKellyJJLoiKWPeakePWUp-regulation of adiponectin, its isoforms and receptors in end-stage kidney diseaseNephrol Dial Transplant200622171810.1093/ndt/gfl552Search in Google Scholar

James MT, Hemmelgarn BR, Tonelli M. Early recognition and prevention of chronic kidney disease. Lancet. 2010; 375:1296–309.JamesMTHemmelgarnBRTonelliMEarly recognition and prevention of chronic kidney diseaseLancet2010375129630910.1016/S0140-6736(09)62004-3Search in Google Scholar

Decreased G. Definition and classification of CKD. Kidney Int. 2013; 3:19–62.DecreasedGDefinition and classification of CKDKidney Int20133196210.1038/kisup.2012.64408969325018975Search in Google Scholar

Levey AS, Eckardt K-U, Tsukamoto Y, Levin A, Coresh J, Rossert J, et al. Definition and classification of chronic kidney disease: a position statement from kidney disease: Improving Global Outcomes (KDIGO). Kidney Int. 2005; 67:2089–100.LeveyASEckardtK-UTsukamotoYLevinACoreshJRossertJet alDefinition and classification of chronic kidney disease: a position statement from kidney disease: Improving Global Outcomes (KDIGO)Kidney Int200567208910010.1111/j.1523-1755.2005.00365.x15882252Search in Google Scholar

Levey AS, Becker C, Inker LA. Glomerular filtration rate and albuminuria for detection and staging of acute and chronic kidney disease in adults: a systematic review. JAMA. 2015; 313:837–46.LeveyASBeckerCInkerLAGlomerular filtration rate and albuminuria for detection and staging of acute and chronic kidney disease in adults: a systematic reviewJAMA20153138374610.1001/jama.2015.0602441036325710660Search in Google Scholar

Inker LA, Astor BC, Fox CH, Isakova T, Lash JP, Peralta CA, et al. KDOQI US commentary on the 2012 KDIGO clinical practice guideline for the evaluation and management of CKD. Am J Kidney Dis. 2014; 63:713–35.InkerLAAstorBCFoxCHIsakovaTLashJPPeraltaCAet alKDOQI US commentary on the 2012 KDIGO clinical practice guideline for the evaluation and management of CKDAm J Kidney Dis2014637133510.1053/j.ajkd.2014.01.41624647050Search in Google Scholar

Collins AJ, Foley RN, Gilbertson DT, Chen S-C. The state of chronic kidney disease, ESRD, and morbidity and mortality in the first year of dialysis. Clin J Am Soc Nephrol. 2009; 4:5–11.CollinsAJFoleyRNGilbertsonDTChenS-CThe state of chronic kidney disease, ESRD, and morbidity and mortality in the first year of dialysisClin J Am Soc Nephrol2009451110.2215/CJN.0598080919996006Search in Google Scholar

Kidney Disease: Improving Global Outcomes (KDIGO). KDIGO 2012 Clinical Practice Guideline for the evaluation and management of chronic kidney disease. Kidney Int. 2013; 3(Suppl):1–150.Kidney Disease: Improving Global Outcomes (KDIGO). KDIGO2012Clinical Practice Guideline for the evaluation and management of chronic kidney diseaseKidney Int20133Suppl1150Search in Google Scholar

Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF, Feldman HI, et al. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009; 150:604–12.LeveyASStevensLASchmidCHZhangYLCastroAFFeldmanHIet alA new equation to estimate glomerular filtration rateAnn Intern Med20091506041210.7326/0003-4819-150-9-200905050-00006276356419414839Search in Google Scholar

Inker LA, Schmid CH, Tighiouart H, Eckfeldt JH, Feldman HI, Greene T, et al. Estimating glomerular filtration rate from serum creatinine and cystatin C. N Engl J Med. 2012; 367:20–9.InkerLASchmidCHTighiouartHEckfeldtJHFeldmanHIGreeneTet alEstimating glomerular filtration rate from serum creatinine and cystatin CN Engl J Med201236720910.1056/NEJMoa1114248439802322762315Search in Google Scholar

World Health Organization. Obesity: preventing and managing the global epidemic: report of a WHO consultation. World Health Organ Tech Rep Ser. 2000; 894:1–253.World Health OrganizationObesity: preventing and managing the global epidemic: report of a WHO consultationWorld Health Organ Tech Rep Ser20008941253Search in Google Scholar

Perri A, Vizza D, Lofaro D, Gigliotti P, Leone F, Brunelli E, et al. Adiponectin is expressed and secreted by renal tubular epithelial cells. J Nephrol. 2013; 26:1049–54.PerriAVizzaDLofaroDGigliottiPLeoneFBrunelliEet alAdiponectin is expressed and secreted by renal tubular epithelial cellsJ Nephrol20132610495410.5301/jn.500026923553527Search in Google Scholar

Wolfson N, Gavish D, Matas Z, Boaz M, Shargorodsky M. Relation of adiponectin to glucose tolerance status, adiposity, and cardiovascular risk factor load. Exp Diabetes Res. 2012; 2012:1–5.WolfsonNGavishDMatasZBoazMShargorodskyMRelation of adiponectin to glucose tolerance status, adiposity, and cardiovascular risk factor loadExp Diabetes Res201220121510.1155/2012/250621325510622253614Search in Google Scholar

Genuth S, Alberti KG, Bennett P, Buse J, Defronzo R, Kahn R, et al. Follow-up report on the diagnosis of diabetes mellitus. Diabetes Care. 2003; 26:3160–7.GenuthSAlbertiKGBennettPBuseJDefronzoRKahnRet alFollow-up report on the diagnosis of diabetes mellitusDiabetes Care2003263160710.2337/diacare.26.11.316014578255Search in Google Scholar

Briffa JF, McAinch AJ, Poronnik P, Hryciw DH. Adipokines as a link between obesity and chronic kidney disease. Am J Physiol Renal Physiol. 2013; 305:1629–36.BriffaJFMcAinchAJPoronnikPHryciwDHAdipokines as a link between obesity and chronic kidney diseaseAm J Physiol Renal Physiol201330516293610.1152/ajprenal.00263.201324107418Search in Google Scholar

Ix JH, Sharma K. Mechanisms linking obesity, chronic kidney disease, and fatty liver disease: the roles of fetuin-A, adiponectin, and AMPK. J Am Soc Nephrol. 2010; 21:406–12.IxJHSharmaKMechanisms linking obesity, chronic kidney disease, and fatty liver disease: the roles of fetuin-A, adiponectin, and AMPKJ Am Soc Nephrol2010214061210.1681/ASN.2009080820447325420150538Search in Google Scholar

Hall JE. The kidney, hypertension, and obesity. Hypertension. 2003; 41:625–33.HallJEThe kidney, hypertension, and obesityHypertension2003416253310.1161/01.HYP.0000052314.95497.7812623970Search in Google Scholar

Eglit T, Lember M, Ringmets I, Rajasalu T. Gender differences in serum high-molecular-weight adiponectin levels in metabolic syndrome. Eur J Endocrinol. 2013; 168:385–91.EglitTLemberMRingmetsIRajasaluTGender differences in serum high-molecular-weight adiponectin levels in metabolic syndromeEur J Endocrinol20131683859110.1530/EJE-12-068823230211Search in Google Scholar

Cnop M, Havel P, Utzschneider K, Carr D, Sinha M, Boyko E, et al. Relationship of adiponectin to body fat distribution, insulin sensitivity and plasma lipoproteins: evidence for independent roles of age and sex. Diabetologia. 2003; 46:459–69.CnopMHavelPUtzschneiderKCarrDSinhaMBoykoEet alRelationship of adiponectin to body fat distribution, insulin sensitivity and plasma lipoproteins: evidence for independent roles of age and sexDiabetologia2003464596910.1007/s00125-003-1074-z12687327Search in Google Scholar

Nishizawa H, Shimomura I, Kishida K, Maeda N, Kuriyama H, Nagaretani H, et al. Androgens decrease plasma adiponectin, an insulin-sensitizing adipocyte-derived protein. Diabetes. 2002; 51:2734–41.NishizawaHShimomuraIKishidaKMaedaNKuriyamaHNagaretaniHet alAndrogens decrease plasma adiponectin, an insulin-sensitizing adipocyte-derived proteinDiabetes20025127344110.2337/diabetes.51.9.273412196466Search in Google Scholar

Mamaghani F, Zarghami N, Maleki M, Pourhassan MM, Hosseinpanah F. Variation of adiponectin levels in normal and obese subjects: possible correlation with lipid profiles. Int J Endocrinal Metab. 2009; 3:170–8.MamaghaniFZarghamiNMalekiMPourhassanMMHosseinpanahFVariation of adiponectin levels in normal and obese subjects: possible correlation with lipid profilesInt J Endocrinal Metab200931708Search in Google Scholar

Shoji T, Shinohara K, Hatsuda S, Kimoto E, Fukumoto S, Emoto M, et al. Altered relationship between body fat and plasma adiponectin in end-stage renal disease. Metab Clin Exp. 2005; 54:330–4.ShojiTShinoharaKHatsudaSKimotoEFukumotoSEmotoMet alAltered relationship between body fat and plasma adiponectin in end-stage renal diseaseMetab Clin Exp200554330410.1016/j.metabol.2004.09.01215736110Search in Google Scholar

Obata Y, Yamada Y, Takahi Y, Baden MY, Saisho K, Tamba S, et al. Relationship between serum adiponectin levels and age in healthy subjects and patients with type 2 diabetes. Clin Endocrinol. 2013; 79:204–10.ObataYYamadaYTakahiYBadenMYSaishoKTambaSet alRelationship between serum adiponectin levels and age in healthy subjects and patients with type 2 diabetesClin Endocrinol2013792041010.1111/cen.1204122963459Search in Google Scholar

Christou GA, Tellis K, Elisaf M, Tselepis AD, Kiortsis DN. High density lipoprotein is positively correlated with the changes in circulating total adiponectin and high molecular weight adiponectin during dietary and fenofibrate treatment. Hormones. 2012; 11:178.ChristouGATellisKElisafMTselepisADKiortsisDNHigh density lipoprotein is positively correlated with the changes in circulating total adiponectin and high molecular weight adiponectin during dietary and fenofibrate treatmentHormones20121117810.14310/horm.2002.134522801564Search in Google Scholar

Tedla F, Brar A, Browne R, Brown C. Hypertension in chronic kidney disease: navigating the evidence. Int J Hypertens. 2011; 2011:1–9.TedlaFBrarABrowneRBrownCHypertension in chronic kidney disease: navigating the evidenceInt J Hypertens201120111910.4061/2011/132405312425421747971Search in Google Scholar

Monhart V. Hypertension and chronic kidney diseases. Cor Vasa. 2013; 55:397–402.MonhartVHypertension and chronic kidney diseasesCor Vasa20135539740210.1016/j.crvasa.2013.07.006Search in Google Scholar

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