Vettoretti Simone, Caldiroli Lara, Molinari Paolo, Villa Amanda, Corsi Romanelli Massimiliano M, Vianello Elena, Dozio Elena, Genovesi Simonetta
Unit of Nephrology and Dialysis Fondazione IRCCS San Gerardo di Monza, 20900 Monza, Italy.
School of Medicine and Surgery, University of Milan Bicocca, 20126 Milan, Italy.
Metabolites. 2025 Aug 1;15(8):515. doi: 10.3390/metabo15080515.
Chronic kidney disease (CKD) increases cardiovascular risk through mechanisms such as oxidative stress and the accumulation of advanced glycation end products (AGEs). Glycated albumin (GA) is associated with cardiovascular risk in CKD patients, but its relationship with AGEs and systemic inflammation remains unclear. This study investigated these associations in old patients with severe CKD, with and without diabetes.
We conducted a cross-sectional analysis in 122 patients aged ≥ 65 years with CKD stages G3a-G5, including 67 diabetics and 55 non-diabetics. Patients with confounding comorbidities were excluded. We measured GA, AGEs, various AGEs receptors (RAGE) isoforms, and inflammatory cytokines (CRP, IL-6, TNFα, and MCP-1) using standardized assays. Statistical analyses included group comparisons, correlation coefficients, and multivariate regression.
Of 122 patients (mean age 77.7 ± 11.3 years), diabetics had higher GA percentages than non-diabetics (22.0 ± 7.1% vs. 17.5 ± 5.4%, = 0.0001), while AGEs (2931 ± 763 vs. 3156 ± 809 AU; = 0.118) and inflammatory markers (CRP 0.240[0.380] vs. 0.200[0.280] mg/dL; = 0.142; IL-6 3.4[4.0] vs. 3.0[3.8] pg/mL; = 0.238) were similar between groups. Overall, GA was inversely correlated with estimated glomerular filtration rate (eGFR) (ρ = -0.189, = 0.037) and positively with glycated hemoglobin (HbA1c) (ρ = 0.525, < 0.0001), but showed no significant correlation with AGEs, RAGE isoforms, or inflammatory cytokines. In multivariate analysis, only HbA1c remained independently associated with GA (β = 0.222, = 0.005).
In old patients with severe CKD, GA appears to be a more useful marker of glycemic control than glycation stress, the latter of which is the result of multiple factors, including impaired kidney function and systemic inflammation.
慢性肾脏病（CKD）通过氧化应激和晚期糖基化终产物（AGEs）积累等机制增加心血管疾病风险。糖化白蛋白（GA）与CKD患者的心血管疾病风险相关，但其与AGEs及全身炎症的关系尚不清楚。本研究调查了老年重度CKD患者（无论有无糖尿病）中的这些关联。
我们对122例年龄≥65岁、CKD分期为G3a - G5期的患者进行了横断面分析，其中包括67例糖尿病患者和55例非糖尿病患者。排除有混杂合并症的患者。我们使用标准化检测方法测量了GA、AGEs、各种AGEs受体（RAGE）亚型以及炎性细胞因子（CRP、IL - 6、TNFα和MCP - 1）。统计分析包括组间比较、相关系数和多变量回归。
在122例患者（平均年龄77.7±11.3岁）中，糖尿病患者的GA百分比高于非糖尿病患者（22.0±7.1%对17.5±5.4%，P = 0.0001），而AGEs（2931±763对3156±809 AU；P = 0.118）和炎性标志物（CRP 0.240[0.380]对0.200[0.280]mg/dL；P = 0.142；IL - 6 3.4[4.0]对3.0[3.8]pg/mL；P = 0.238）在两组间相似。总体而言，GA与估计肾小球滤过率（eGFR）呈负相关（ρ = - 0.189，P = 0.037），与糖化血红蛋白（HbA1c）呈正相关（ρ = 0.525，P < 0.0001），但与AGEs、RAGE亚型或炎性细胞因子无显著相关性。在多变量分析中，只有HbA1c与GA独立相关（β = 0.222，P = 0.005）。
在老年重度CKD患者中，GA似乎比糖基化应激更能有效反映血糖控制情况，糖基化应激是包括肾功能受损和全身炎症在内的多种因素导致的结果。
