慢性肾脏病血管钙化的药物干预：随机对照试验的系统评价与荟萃分析。
完整摘要 · 中文译文
目的 评估药物干预对慢性肾病患者血管钙化及相关结局的疗效。方法 检索PubMed、Embase、Web of Science和Cochrane Library，检索时间从建库至2026年5月1日。纳入比较药物干预与安慰剂、标准治疗或其他对照在慢性肾病患者中的随机对照试验。主要结局为影像学定义的血管钙化指标，包括冠状动脉钙化Agatston评分、冠状动脉钙化进展百分比、冠状动脉钙化体积变化和腹主动脉钙化进展。次要结局包括颈动脉内膜中层厚度、血清钙化倾向（T50）、动脉僵硬度、钙化相关生物标志物、矿物质代谢参数和全因死亡率。采用均数差或比值比及95%置信区间，根据异质性使用固定效应模型或随机效应模型进行合并。结果 共纳入28项随机对照试验，涉及6330名受试者。药物干预未显著降低冠状动脉钙化Agatston评分、冠状动脉钙化进展、冠状动脉钙化体积变化、腹主动脉钙化进展、动脉僵硬度或全因死亡率。左侧颈动脉内膜中层厚度（均数差 -0.06 mm，95%置信区间：-0.10至-0.02）和颈总动脉 内膜-中层厚度（平均差 -0.07 mm，95% 置信区间：-0.14 至 -0.00）、T50 变化（平均差 50.25 min，95% 置信区间：34.68-65.82）以及脱磷酸化-未羧化基质 Gla 蛋白（平均差 -504.97 pmol/L，95% 置信区间：-789.72 至 -220.22）。大多数矿物质代谢参数无变化，尽管离子钙轻度降低。效应因药理学策略而异，支持针对特定干预措施的解释。结论：药理学干预在慢性肾病患者影像学定义的血管钙化方面未显示出一致获益。T50、脱磷酸化-未羧化基质 Gla 蛋白以及选定的颈动脉内膜-中层厚度指标的改善提示存在通路特异性的生物学或血管效应，这些效应可能先于结构性钙化减少，或不能直接转化为结构性钙化减少。需要采用标准化影像学终点、更长随访时间以及临床相关亚组报告的进一步随机对照试验，以确定哪些治疗策略能提供有意义的血管获益。
完整摘要 · 英文原文
ObjectiveTo evaluate the efficacy of pharmacological interventions for vascular calcification and related outcomes in patients with chronic kidney disease.MethodsPubMed, Embase, Web of Science, and the Cochrane Library were searched from inception to 1 May 2026. Randomized controlled trials comparing pharmacological interventions with placebo, standard care, or other controls in patients with chronic kidney disease were included. Primary outcomes were imaging-defined measures of vascular calcification, including coronary artery calcification Agatston score, percentage coronary artery calcification progression, coronary artery calcification volume change, and abdominal aortic calcification progression. Secondary outcomes included carotid intima-media thickness, serum calcification propensity (T50), arterial stiffness, calcification-related biomarkers, mineral metabolism parameters, and all-cause mortality. Mean differences or odds ratios with 95% confidence intervals were pooled using fixed- or random-effects models according to heterogeneity.ResultsTwenty-eight randomized controlled trials involving 6330 participants were included. Pharmacological interventions did not significantly reduce the coronary artery calcification Agatston score, coronary artery calcification progression, coronary artery calcification volume change, abdominal aortic calcification progression, arterial stiffness, or all-cause mortality. Significant effects were observed for left carotid intima-media thickness (mean difference -0.06 mm, 95% confidence interval: -0.10 to -0.02), common carotid artery intima-media thickness (mean differences -0.07 mm, 95% confidence interval: -0.14 to -0.00), T50 change (mean differences 50.25 min, 95% confidence interval: 34.68-65.82), and dephosphorylated-uncarboxylated matrix Gla protein (mean differences -504.97 pmol/L, 95% confidence interval: -789.72 to -220.22). Most mineral metabolism parameters were unchanged, although ionized calcium was modestly reduced. Effects varied by pharmacological strategy, supporting intervention-specific interpretation.ConclusionsPharmacological interventions did not show consistent benefits on imaging-defined vascular calcification in patients with chronic kidney disease. Improvements in T50, dephosphorylated-uncarboxylated matrix Gla protein, and selected carotid intima-media thickness measures suggest pathway-specific biological or vascular effects that may precede or not directly translate into reduced structural calcification. Further randomized controlled trials with standardized imaging endpoints, longer follow-up, and clinically relevant subgroup reporting are needed to determine which therapeutic strategies provide meaningful vascular benefits.