Nephrology Division of Federal University of São Paulo, Rua Pedro de Toledo, 282 - Vila Clementino, São Paulo, SP, 04039-000, Brazil.
Heart Institute of the University of São Paulo, Av. Dr. Enéas Carvalho de Aguiar, 44 - Pacaembu, São Paulo, SP, 05403-900, Brazil.
BMC Nephrol. 2020 Apr 6;21(1):121. doi: 10.1186/s12882-020-01756-2.
Vascular calcification progression has been associated with the loss of trabecular bone in chronic kidney disease (CKD) patients. There are few data evaluating the relationship between cortical bone loss and vascular calcification in this population. The aim of this study was to prospectively evaluate the association between changes in cortical bone density and coronary artery calcification (CAC) progression in non-dialyzed CKD patients.
Changes of cortical and trabecular bone, and changes of calcium score, were analyzed using vertebral tomographic images from a prospective study. Automatic delineation of the cortical bone layer was performed by Image J software, and trabecular bone was determined by selecting a region of interest using Vitrea 2® software. Cortical and trabecular bone density (BD) were expressed in Hounsfield Units (HU), and coronary artery calcium score in Agatston Units (AU).
Seventy asymptomatic patients [57.8 ± 10.2 years, 63% males, 20% diabetic, estimated glomerular filtration rate (eGFR) = 37.3 (24.8-51.3) mL/min/1.73m] were followed for 24 months. The mean cortical and trabecular BD did not change over time. While 49 patients lost either bone, 29 (41%) patients lost cortical [- 4.4%/year (ranging from - 7.15 to - 0.5)] and 39 (56%) lost trabecular bone [- 3.15%/year (- 13.7 to - 0.25)]. There was no association between cortical and trabecular BD changes (p = 0.12). CAC was observed in 33 (46%) patients at baseline, and 30 (91%) of them showed CAC progression. While an inverse correlation between trabecular bone and calcium score changes was observed (p = 0.001), there was no correlation between cortical bone and calcium score changes (p = 0.34).
CKD patients experience either cortical or trabecular bone loss over time, but these changes do not take place simultaneously in all patients. Cortical, unlike trabecular bone loss, is not associated with vascular calcification progression in these patients.
血管钙化进展与慢性肾脏病(CKD)患者的小梁骨丢失有关。在该人群中,评估皮质骨丢失与血管钙化之间关系的数据很少。本研究的目的是前瞻性评估非透析 CKD 患者皮质骨密度变化与冠状动脉钙化(CAC)进展之间的关系。
使用前瞻性研究的椎体断层图像分析皮质骨和小梁骨的变化,以及钙评分的变化。使用 Image J 软件自动勾画皮质骨层,使用 Vitrea 2®软件选择感兴趣区域来确定小梁骨。皮质骨和小梁骨密度(BD)用亨氏单位(HU)表示,冠状动脉钙评分用 Agatston 单位(AU)表示。
70 例无症状患者[57.8±10.2 岁,63%为男性,20%为糖尿病患者,估算肾小球滤过率(eGFR)=37.3(24.8-51.3)mL/min/1.73m]随访 24 个月。皮质和小梁骨的平均 BD 随时间没有变化。49 例患者中有 29 例(41%)同时丢失皮质骨[每年-4.4%(范围为-7.15 至-0.5)],39 例(56%)丢失小梁骨[每年-3.15%(范围为-13.7 至-0.25)]。皮质和小梁骨 BD 的变化之间没有相关性(p=0.12)。基线时有 33 例(46%)患者存在 CAC,其中 30 例(91%)患者 CAC 进展。虽然观察到小梁骨与钙评分变化之间存在负相关(p=0.001),但皮质骨与钙评分变化之间没有相关性(p=0.34)。
随着时间的推移,CKD 患者会出现皮质骨或小梁骨丢失,但并非所有患者同时出现这些变化。与小梁骨丢失不同,皮质骨丢失与这些患者的血管钙化进展无关。