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

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. © American Journal of Hypertension, Ltd 2015. All rights reserved. For Permissions, please email: journals.permissions@oup.com.