Renal vasodilating capacity and endothelial function are impaired in patients with obstructive sleep apnea syndrome and no traditional cardiovascular risk factors

Abstract

Objective: Patients with obstructive sleep apnea syndrome exhibit accelerated vascular aging and renal damage. Aim of the study was to investigate whether vascular dysfunction is a feature of obstructive sleep apnea syndrome per se or instead related to the presence of traditional cardiovascular risk factors.Methods: Forty patients with moderate-severe obstructive sleep apnea syndrome (20 with, 20 without traditional risk factors) and 20 matched healthy controls were enrolled. Renal vasodilating capacity, endothelium-dependent vasodilation in the brachial artery, carotid-femoral pulse wave velocity and carotid stiffness were measured. Oxidative stress, endothelial biomarkers and leukocyte adhesion molecule levels were also evaluated.Results: Apneic patients without traditional cardiovascular risk factors presented reduced endothelium-dependent vasodilation (3.7 AE 2.1 versus 6.1 AE 3.0%, P < 0.05), increased serum E-selectin (49.8 AE 11.5 versus 38.9 AE 17.9 ng/ml, P < 0.05), and impaired renal vasodilating capacity (6.0 AE 4.3 versus 10.4 AE 6.1%, P < 0.05), as compared to healthy controls. Endothelial NO synthase expression was reduced (0.0133 versus 0.0221 Â 10 6 copies/mg RNA, P < 0.05), whereas oxidative stress parameters and leukocyte adhesion molecules were similar to controls. Patients with obstructive sleep apnea syndrome and traditional risk factors also exhibit increased aortic and carotid stiffness, increased renal resistive index and intima-media thickness, and reduced expression of the endothelial progenitor cell marker CD34: however, these parameters were similar to those of healthy controls in patients with isolated obstructive sleep apnea syndrome.Conclusion: Obstructive sleep apnea syndrome is characterized by endothelial dysfunction and activation and impaired renal vasodilating capacity even in the absence of traditional cardiovascular risk factors, possibly due to reduced endothelial NO synthase expression.

An update on cardiovascular effects of obstructive sleep apnoea syndrome

“…In one of our studies, we also demonstrated that oxidative stress markers are increased and antioxidant enzymes are reduced in patients with OSA 25. Brachial artery diameters are found to be greater in patients with OSA compared with controls 26. Endothelial NOS, which is associated with vasodilatation, is reduced in patients with OSA and may contribute to endothelial dysfunction.…”

Association between Obstructive Sleep Apnea and Acute Kidney Injury in Critically Ill Patients: A Propensity-Matched Study

“…Increased inflamma- tory cytokines and subsequent endothelial cell dysfunction can contribute to the development and progression of AKI. So, it could be hypothesized that episodes of apnea during sleep could result in repeated subclinical tubular cell injuries, which predispose patients to AKI, particularly when a second insult occurs in ICU [13,45] . In addition, there is a well-described association among OSA with pulmonary and systemic HTN [46] .…”

Emerging co-morbidities of obstructive sleep apnea: cognition, kidney disease, and cancer

“…In a study comparing healthy controls with newly diagnosed patients with moderate to severe OSA, but free of cardiovascular risk factors, the OSA patients showed evidence of endothelial dysfunction, impaired renal vasodilation and reduced endothelial nitric oxide synthase expression, despite a lack of overt signs of end organ disease. This suggests that OSA in itself is an independent risk factor for clinically occult renal endothelial damage which is not clinically detectible, which may then proceed to overt renal dysfunction (95).…”