Abstract: FR-PO0367
Highlighting the Cardiorenal Complications from Endothelin, Inflammation, and Fibrosis in Patients with Resistant Hypertension with and Without CKD
Session Information
- Hypertension and CVD: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1602 Hypertension and CVD: Clinical
Authors
- Rathi, Hinal, UAB Huntsville Regional Campus, Huntsville, Alabama, United States
- Pathak, Prutha, North Alabama Medical Center, Florence, Alabama, United States
- Dudenbostel, Tanja, UAB Huntsville Regional Campus, Huntsville, Alabama, United States
Background
Endothelin-1 (ET-1) is a potent peptide associated with hypertension (HTN) and chronic kidney disease (CKD). ET-1 primarily acts through two receptors: ETA and ETB. Activation of ETA receptors leads to sodium retention, vasoconstriction, inflammation, fibrosis, and various downstream effects in the renal system. This study not only explores the interaction between ET-1 and inflammation as an additional potential pathway for CKD progression to end-stage renal disease (ESRD) but also aims to assess the risk for cardiovascular kidney metabolic (CKM) syndrome by measuring myocardial fibrosis and body mass index (BMI) in resistant hypertension (RHTN) patients with and without CKD.
Methods
We conducted a cross-sectional analysis of 133 patients, 100 without CKD and 33 with CKD stages 2 and 3, referred to the RHTN Clinic at the University of Alabama, Birmingham. In addition to the plasma ET-1, C-reactive protein, C-terminal propeptide of type I collagen (CICP), ICTP (carboxy-terminal telopeptide of type I collagen) markers for myocardial fibrosis, and BMI were measured.
Results
Overall, the RHTN cohort with and without CKD tended to be older than the control group (55.3±10.9 vs 49.4±8.1 years, p = 0.005). CKD stages 2 and 3 were more prevalent among males, African Americans, and were less obese. Patients in the RHTN cohort with CKD stages 2 and 3 had higher ET-1 levels than patients without CKD (10.0 ± 9.64 vs 7.3 ± 4.9 pg/mL, p =0.12). Likewise, in the same cohort, CKD stages 2 and 3 patients had a trend of higher CRP (9.03 ± 18.28 vs 6.69 ± 7.27 mg/L, p=0.53) and ICTP (3.93 ±1.75 vs 3.47 ±1.55 ng/mL, p=0.40) but lower CICP (56.26 ±25.55 vs 67.07± 27.33 ng/mL, p=0.21) than non-CKD patients.
Conclusion
Age and ET-1 were associated with an increased risk of CKD in RHTN. Increasing BMI was associated with decreased odds of CKD in RHTN. Myocardial fibrosis markers CICP and ICTP, along with CRP levels, did not show any significant association with the odds of developing CKD in RHTN. This can be attributed to the study size. Overall, this not only potentiates the need to replicate this study in a larger sample size but also investigates the role of endothelin antagonists, anti-fibrotic drugs, in delaying the progression of CKD in patients with RHTN and avoiding metabolic syndromes.