Abstract
Individuals with chronic kidney disease are at an increased risk for cardiovascular disease. This risk may partially be explained by a chronic inflammatory state in these patients, reflected by increased arterial wall and cellular inflammation. Statin treatment decreases cardiovascular risk and arterial inflammation in non-CKD subjects. In patients with declining kidney function, cardiovascular benefit resulting from statin therapy is attenuated, possibly due to persisting inflammation. In the current study, we assessed the effect of statin treatment on arterial wall and cellular inflammation. Fourteen patients with chronic kidney disease stage 3 or 4, defined by an estimated Glomerular Filtration Rate between 15 and 60 mL/min/1.73 m2, without cardiovascular disease were included in a single center, open label study to assess the effect of atorvastatin 40 mg once daily for 12 weeks (NTR6896). At baseline and at 12 weeks of treatment, we assessed arterial wall inflammation by 18F-fluoro-deoxyglucose positron-emission tomography computed tomography (18F-FDG PET/CT) and the phenotype of circulating monocytes were assessed. Treatment with atorvastatin resulted in a 46% reduction in LDL-cholesterol, but this was not accompanied by an attenuation in arterial wall inflammation in the aorta or carotid arteries, nor with changes in chemokine receptor expression of circulating monocytes. Statin treatment does not abolish arterial wall or cellular inflammation in subjects with mild to moderate chronic kidney disease. These results imply that CKD-associated inflammatory activity is mediated by factors beyond LDL-cholesterol and specific anti-inflammatory interventions might be necessary to further dampen the inflammatory driven CV risk in these subjects.
Highlights
Individuals with chronic kidney disease are at an increased risk for cardiovascular disease
The association between LDL-cholesterol and CV risk is attenuated compared to the non-Chronic kidney disease (CKD) population[8], resulting in a decreased beneficial impact of statin therapy as the estimated glomerular filtration rate declines[6]
We demonstrated that subjects with mild to moderate CKD have increased arterial wall inflammation compared to healthy controls as assessed by 18F-FDG positron emission tomography/ computed tomography (PET/CT)[10]
Summary
Individuals with chronic kidney disease are at an increased risk for cardiovascular disease. Statin treatment does not abolish arterial wall or cellular inflammation in subjects with mild to moderate chronic kidney disease. These results imply that CKD-associated inflammatory activity is mediated by factors beyond LDL-cholesterol and specific anti-inflammatory interventions might be necessary to further dampen the inflammatory driven CV risk in these subjects. The association between LDL-cholesterol and CV risk is attenuated compared to the non-CKD population[8], resulting in a decreased beneficial impact of statin therapy as the estimated glomerular filtration rate (eGFR) declines[6]. We investigated the extent of statin-mediated lowering of inflammatory activity in subjects with CKD To this end, we assessed arterial wall inflammation and monocyte phenotype before and after 3 months of potent statin treatment in subjects with stage 3 or 4 CKD
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
