目的 探究血清肝激酶B1(liver kinase B1，LKB1)水平与腹膜透析(peritoneal dialysis,PD)患者血管钙化的相关性。 方法 纳入2022年9月─2023年9月在青岛市市立医院肾内科行规律PD治疗≥3个月的78例患者作为研究对象。收集入选者的临床资料及实验室化验指标；ELISA测定血清LKB1水平；腹部侧位X线平片评估血管钙化程度及腹主动脉钙化积分(abdominal aortic calcification score,ACCs)。Spearman相关性分析、多元线性回归分析PD患者血清LKB1水平的影响因素； Logistic回归分析PD患者腹主动脉钙化(abdominal aortic calcification,ACC)的危险因素。 结果 PD患者的血清LKB1水平低于健康对照组(Z=-4.393,P＜0.001)。LKB1水平与PD患者的年龄、透析龄、甲状旁腺激素、三酰甘油、AACs呈负相关(rs=-0.262、-0.227、-0.293、-0.259、-0.611，P=0.021，0.046、0.009、0.022、＜0.001)。多元线性回归分析示甲状旁腺激素和AACs是LKB1的独立影响因素(β=-0.208、 -0.519，P=0.042、＜0.001)。Logistic回归分析示血清高LKB1水平是PD患者发生AAC的独立保护因素(OR=0.961，95% CI：0.936～0.986，P=0.003)。ROC曲线分析LKB1预测PD患者发生中-重度AAC的AUC为0.812(95% CI:0.719～0.905，P＜0.001)，最佳截断值为115.68 ng/L，敏感度为0.622，特异性为0.854，约登指数为0.476。 结论 PD患者的血清LKB1水平低于健康对照组，且与AAC相关。
Objective To explore the relationship between serum liver kinase B1 (LKB1) level and vascular calcification in peritoneal dialysis (PD) patients. Methods A total of 78 patients (≥ 3 month) who were treated with PD in the Department of Nephrology of Qingdao Municipal Hospital from September 2022 to September 2023 were included in the study. Collect the clinical data and laboratory indicators of Finalists; ELISA was used to detect the serum LKB1 level; the degree of vascular calcification and the abdominal aortic calcification score (ACCs) was evaluated by abdominal lateral X-ray plain film. Spearman correlation analysis and multiple linear regression analysis of influencing factors of serum LKB1 level in patients with PD; the influencing factors for serum LKB1 level were evaluated by Spearman correlation analysis and multivariate linear regression, and the influencing factors for abdominal aortic calcification score (AAC) in PD patients were assessed by Logistic regression. Results Serum LKB1 level was lower in the PD patients than in the healthy controls (Z=-4.393，P<0.001). LKB1 level was negatively correlated with age, dialysis age, PTH, triglyceride and AACs (r=-0.262，-0.227，-0.293，-0.259，-0.611; P=0.021，0.046，0.009，0.022，＜0.001). Multivariate linear regression showed that PTH and AACs were the independent influencing factors for serum LKB1 level (β=-0.208, -0.519; P=0.042，＜0.001). Logistic regression analysis demonstrated that high serum LKB1 level was an independent protective factor for AAC in PD patients (OR,95% CI：0.961 (0.936, 0.986), P=0.003). ROC-AUC of serum LKB1 for moderate to severe AAC was 0.812 (95% CI：0.719～0.905, P＜0.001), cut-off value 115.68ng/L, sensitivity 0.622, and specificity 0.854, the Yoden index is 0.476. Conclusions Serum LKB1 level in PD patients is lower than that in healthy people, and was associated with the AAC.
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