Serum progranulin/tumor necrosis factor-α ratio as independent predictor of systolic blood pressure in overweight hypertensive patients: a cross-sectional study

Abstract

Background: Vascular inflammation plays a key role in the progression of hypertension. Progranulin (PGRN), an anti-inflammatory growth factor, mediated inhibition of tumor necrosis factor-α (TNF-α), a pleiotropic cytokine, activity has been well-established. Despite the role of chronic low-grade inflammation in hypertension, serum levels of PGRN and PGRN/TNF-α ratio and, their association with systolic and diastolic blood pressure has not been determined in hypertensive patients till now. This study aims to find and correlate the serum levels of pro-inflammatory cytokine (TNF-α), anti-inflammatory growth factor (PGRN), and PGRN/TNF-α ratio with the blood pressure in systolic-diastolic hypertension (SDH) and isolated systolic hypertension (ISH) patients. Results: A cross-sectional study was conducted on SDH patients (mean age, 52.95 ± 12.6 years; male/female (M/F) number = 15/10) and ISH patients (mean age, 55.80 ± 9.40 years; M/F number = 12/13) (n = 25 each). Twenty-five age and body mass index (BMI)-matched healthy subjects (mean age, 56.00 ± 8.55 years; male/female number = 11/14) were considered as control. All patients and healthy subjects were overweight (BMI, 25–30 kg/m2). Overnight fasting blood samples of subjects were taken and levels of PGRN and TNF-α were measured using ELISA diagnostic kits. PGRN and TNF-α levels were found significantly high, whereas PGRN/TNF ratio was found very low, in SDH and ISH patients as compared to healthy subjects. Reduced PGRN/TNF-α ratio and pulse pressure were found as independent predictors of SBP both in SDH and ISH patients. Conclusions: Findings of elevated PGRN levels in response to raised TNF-α levels depict the counter regulation by PGRN to neutralize TNF-α. Findings of reduced PGRN/TNF ratio, and it being an independent predictor of SBP, ascertain the key role of imbalance in pro- and anti-inflammatory environment in hypertension. Thus, it strengthens the cross-link between the concept of immunity–adiposity–inflammation–blood pressure¸ a vicious network. Further, this cross-link of SBP and progranulin must be explored in longitudinal studies. New researches should be focused not only on impact of pro-inflammatory environment rather to find on a balance between pro- and anti-inflammatory status, so that new target sites could be explored for therapeutic management of hypertension.