Abstract 346: Subcutaneous Resistance Artery Remodeling And Function In Chronic Kidney Disease Patients
Background: Chronic kidney disease (CKD) is associated with cardiovascular (CV) complications. However, interventional trials targeting classical CV risks factors have been often unsuccessful in advanced stage CKD, which emphasizes the need to better understand CKD-associated vascular disorders. Resistance arteries are a key determinant of blood pressure (BP) and their changes in different CV conditions contribute to target organ damage. The aim of the present study was to characterize resistance artery remodeling and function in CKD patients, compared to vessels from hypertensive (HTN) subjects.
Method: Twenty-two stage 4 CKD patients (aged 63.6±3.1 years) and 16 HTN subjects (45.6±16.1 years) were included in the present study. They all underwent a subcutaneous biopsy under local anaesthesia. Small artery remodeling and function were studied on a pressurized myograph, and subcutaneous fat CD3 infiltration and media fibronectin expression by immunostaining. Vascular smooth muscle cells (VSMCs) were counted after hematoxilin-eosin staining.
Results: CKD systolic BP was similar to HTN (133±18 vs. 143±10 mmHg, respectively). Vasodilatory responses to acetylcholine were lower in CKD compared to HTN (maximal relaxation (%), 74.3±3.4 vs. 87.5±2.7, P<0.05). Media/lumen at 60 mmHg was lower in CKD than in HTN (6.7±0.5 vs 8.8±0.7, P<0.05). Resistance artery stiffness was lower in CKD compared to HTN (strain at 120 mmHg, 0.845±0.126 vs 0.585±0.099, P<0.05). Fibronectin staining in resistance arteries was lower in CKD than HTN (8.2±0.8 vs 23.3±1.7 RFU/μm2, P<0.001). Less VSMCs were present in the arterial wall of CKD compared to HTN (5.4±0.4 vs 7.2±0.5 cells/μm2, P<0.05). Subcutaneous fat presented fewer CD3+ cells in CKD than HTN (12.8±4.1 vs 23.7±12.8 cells/mm2, P<0.05).
Conclusion: Despite higher levels of BP, resistance arteries isolated from CKD patients exhibited no vascular remodeling and lower arterial stiffness compared with HTN patients. These results are in line with the maladaptive hypotrophic remodeling observed in large vessels in CKD, suggesting a generalized vascular defect in mechanotransduction in CKD.
Author Disclosures: J.C. Fraulob-Aquino: None. M. Briet: None. T. Barhoumi: None. C. Savoia: None. P. Paradis: None. E.L. Schiffrin: None.
- © 2014 by American Heart Association, Inc.