Objective: Introduction: Refractory hypertension (RfHT) is defined as an uncontrolled blood pressure (BP) despite the use of 5 or more antihypertensives, including spironolactone and it is considered an extreme phenotype of resistant hypertension (RHT). High BP levels lead to RAAS stimulation, sympathetic hyperactivity and endothelial dysfunction with consequent production of pro-inflammatory cytokines. Objective: To evaluate the relationship between inflammatory markers and refractory hypertension in a large cohort of patients with RHT. Design and method: A cross-sectional study that evaluated 423 resistant hypertensives (30.5% male, mean age 63.9 ± 10.8 years), of which 62 (14.6%) diagnosed as RfHT. All of them were submitted to the dosage of inflammatory markers: TNF-alpha, MCP-1, E-selectin and PAI-1. Socio-demographic and anthropometric characteristics and cardiovascular risk factors (CV) were recorded. Variance analysis compared serum levels of the 4 inflammatory markers and bivariate analysis compared patients with RHT versus RfHT. Results: Patients with RfHT are younger, with higher prevalence of smoking, higher levels of albuminuria and higher prevalence of chronic cerebrovascular and renal disease stages 4 and 5. PAI-1 values (126 [108–162] vs 118 [94–153] were higher in those with RfHT, although they did not reach statistical significance. The other biomarkers evaluated showed no association with the diagnosis of RfHT. Conclusions: Among inflammatory markers, PAI-1 was the one that correlated most strongly with refractory hypertension. Our study is the first one to demonstrate PAI-1 association with treatment refractoriness
Objective: Background: Resistant hypertension (RHT) defined as an uncontrolled blood pressure (BP) despite the use of 3 or more antihypertensives presents a high cardiovascular (CV) morbidity and mortality and high prevalence of chronic kidney disease (CKD). High BP levels and kidney injury appear to be strongly associated with inflammatory biomarkers. Objective: To evaluate the relationship between inflammatory markers and subclinical and established CKD in a large cohort of patients with RHT Design and method: Cross-sectional study that evaluated 423 resistant hypertensives (30.5% male, mean age 64.0 ± 10.8 years) submitted to renal function assessment (albuminuria dosage and evaluation of glomerular filtration rate calculated from the CKD-EPI formula) and dosage of inflammatory markers: TNF-alpha, MCP-1, E-selectin and PAI-1. Socio-demographic characteristics, anthropometric measurements and CV risk factors were recorded. We considered subclinical CKD those patients with moderately high albuminuria (30–300 mg/g) and/or GFR between 30 and 60 ml/min/1.73m2 and established CKD those who presented albuminuria > 300 mg/g and/or TFG < 30 ml/min/1.73m2. Variance analysis compared serum levels of the 4 inflammatory markers and bivariate analysis compared patients with and without subclinical and established chronic kidney disease. Results: The prevalence of established CKD was 7.3% (31 patients) and subclinical CKD was 47% (187 patients). Patients with subclinical CKD were older and with higher arterial stiffness (higher pulse wave velocity). TNF-alpha (7.1 [4.4–8.6] vs 51, [3.2–7.5]) and MCP-1(284 [220–379] vs 260 [185–359] were significant higher in this group of patients. When we analyzed patients with established CKD, we observed that they have higher BP levels and that TNF-alpha values (7.8 [5.6–14.0] vs 5.6 [3.5–8.3]) and E-selectin (54.4[41.2–61.3] vs. 47.8 [32.0–65.3]) were significantly higher in this group. Conclusions: Among the inflammatory markers evaluated, which was most strongly correlated with subclinical CKD were TNF-alpha and MCP-1, while those with established CKD have higher TNF-alpha and E-selectin levels, possibly pointing out that the MCP-1 is an earlier marker of kidney injury.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.