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. 2016 Apr;29(4):528-36.
doi: 10.1093/ajh/hpv132. Epub 2015 Aug 22.

Increased Circulating Visfatin Is Associated With Progression of Kidney Disease in Non-Diabetic Hypertensive Patients

Chien-Yi Hsu  1 , Po-Hsun Huang  2 , Tz-Heng Chen  3 , Chia-Hung Chiang  4 , Hsin-Bang Leu  5 , Chin-Chou Huang  6 , Jaw-Wen Chen  6 , Shing-Jong Lin  7
Affiliations

Increased Circulating Visfatin Is Associated With Progression of Kidney Disease in Non-Diabetic Hypertensive Patients

Chien-Yi Hsu et al. Am J Hypertens. 2016 Apr.

Abstract

Backgroud: Declining renal function is an independent risk factor for all-cause mortality in cardiovascular disease. Visfatin has been described as a marker of inflammation and endothelial dysfunction, but whether circulating visfatin levels are predictive to a subsequent decline in renal function remains unclear.

Methods: In total, 200 nondiabetic, non-proteinuric hypertensive outpatients with initial serum creatinine (Scr) ≤1.5 mg/dl were enrolled. Plasma visfatin concentration and endothelial function estimated by brachial artery flow-mediated dilatation (FMD) were determined in the study subjects. The primary endpoints were the occurrence of renal events including doubling of Scr, 25% loss of glomerular filtration rate (GFR) from baseline values, and the occurrence of end-stage renal disease during follow-up.

Results: The mean annual rate of GFR decline (ΔGFR/y) was -1.26±2.76 ml/min/1.73 m(2) per year during follow-up (8.6±2.5 years). At baseline, plasma visfatin was negatively correlated with estimated GFR. In longitudinal analysis, the ΔGFR/y was correlated with visfatin, baseline GFR, FMD, systolic blood pressure, and fasting blood glucose (FBG). Multivariate analysis indicated that increased visfatin (r = -0.331, P <0.001), baseline GFR (r = -0.234, P = 0.001), FMD (r = 0.163, P = 0.015), and FBG (r = -0.160, P = 0.015) are independent predictors of ΔeGFR/y. Cox regression model analysis showed that visfatin (hazard ratio (HR), 1.09; 95% confidence interval (CI), 1.05-1.13, P <0.001), FBG (HR, 1.01; 95% CI, 1.00-1.02, P = 0.020), and FMD (HR, 0.87; 95% CI, 0.76-1.00, P = 0.049) were independently associated with the risk of developing future renal events.

Conclusions: Increased circulating visfatin are associated with subsequent decline in renal function in nondiabetic hypertensive patients.

Keywords: adipokine; blood pressure; chronic kidney disease; endothelial dysfunction; hypertension; visfatin..

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Figures

Figure 1.
Figure 1.
Study protocol and profile.
Figure 2.
Figure 2.
The relationship between circulation visfatin levels and the longitudinal changes in renal function among 200 hypertensive patients. (A) Plasma visfatin levels in low (<75ml/min) and high (≥75ml/min) glomerular filtration rate (GFR) groups (independent t-test P = 0.028). The median of the baseline eGFR was 75.8ml/min/1.73 m2 and a convenient eGFR cutoff value set at 75ml/min was used to classify the study cohort into 2 groups (N = 102 and 98 in each group, respectively). (B) Plasma visfatin levels among individuals with and without renal events (independent t-test P = 0.002). (C) The eGFR change before and after longitudinal follow-up (paired t-test P < 0.001) and data distribution. (D) The annual rate of eGFR decline in the study groups stratified by plasma visfatin levels. All patients were divided into 4 groups according to plasma visfatin levels in quartiles: group 1 (Q1), with visfatin level ≤9.7ng/ml; group 2 (Q2), with visfatin level >9.7ng/ml and ≤11.0ng/ml; group 3 (Q3), with visfatin level >11.0ng/ml and ≤15.8ng/ml; group 4 (Q4), with visfatin level >15.8ng/ml.
Figure 3.
Figure 3.
Kaplan–Meier estimates of survival free of renal events, including doubling of serum creatinine from baseline values, 25% loss of glomerular filtration rate from baseline values, and the occurrence of end-stage renal disease in subjects categorized by visfatin level.
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