Department of Vascular Medicine, Amsterdam University Medical Centers, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands.
Department of Radiology and Nuclear Medicine, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.
Sci Rep. 2021 Feb 18;11(1):4126. doi: 10.1038/s41598-021-83273-2.
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 m, 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 F-fluoro-deoxyglucose positron-emission tomography computed tomography (F-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.
患有慢性肾病的个体发生心血管疾病的风险增加。这种风险可能部分可以通过这些患者的慢性炎症状态来解释，表现为动脉壁和细胞炎症增加。他汀类药物治疗可降低非慢性肾脏病患者的心血管风险和动脉炎症。在肾功能下降的患者中，他汀类药物治疗的心血管获益减弱，可能是由于持续存在的炎症。在当前的研究中，我们评估了他汀类药物治疗对动脉壁和细胞炎症的影响。14 名患有慢性肾脏病 3 或 4 期的患者（定义为估计肾小球滤过率为 15 至 60ml/min/1.73m 之间），无心血管疾病，参与了一项单中心、开放标签研究，以评估阿托伐他汀 40mg 每日一次治疗 12 周（NTR6896）的效果。在基线和治疗 12 周时，我们通过 F-氟代脱氧葡萄糖正电子发射断层扫描计算机断层扫描（F-FDG PET/CT）评估动脉壁炎症，并评估循环单核细胞的表型。阿托伐他汀治疗可使 LDL-胆固醇降低 46%，但这并没有减轻主动脉或颈动脉的动脉壁炎症，也没有改变循环单核细胞趋化因子受体的表达。他汀类药物治疗并不能消除轻度至中度慢性肾脏病患者的动脉壁或细胞炎症。这些结果表明，CKD 相关的炎症活性是由 LDL-胆固醇以外的因素介导的，可能需要特定的抗炎干预措施来进一步降低这些患者的炎症驱动的心血管风险。
