Liu Hai-Long, Zeng Qing-Tian, Xu Yuan-Yuan, Zhang Xiang-Tao, Li Ning, Liang Ning-Peng, Dong Yi-Fei
Department of Cardiovascular Medicine, The 2nd Affiliated Hospital, Jiangxi Medical College, Nanchang University, Jiangxi, China.
Department of Cardiovascular Medicine, Jiu Jiang No.1 People's Hospital, Jiujiang, Jiangxi, China.
J Clin Hypertens (Greenwich). 2025 Aug;27(8):e70124. doi: 10.1111/jch.70124.
Primary aldosteronism (PA) independently increases renal impairment risk beyond blood pressure effects. Although hyperaldosteronism is known to mediate renal injury, associations between plasma aldosterone concentration (PAC) and early kidney damage biomarkers such as retinol-binding protein (RBP) and β2-microglobulin (β2-MG) remain insufficiently explored. We investigated the association of PAC with renal function indicators-including RBP, β2-MG, albumin-to-creatinine ratio (ACR), and estimated glomerular filtration rate (eGFR)-comparing matched patients with PA and essential hypertension (EH). In this cross-sectional study, 546 PA patients and 546 propensity score-matched EH patients were assessed. Spearman correlations and multivariate regression analyses assessed PAC-renal marker associations, with interactions tested to determine differences between PA and EH groups. In PA, PAC strongly correlated with lower eGFR (r = -0.597, p < 0.001) and higher RBP (r = 0.559), β2-MG (r = 0.632), and ACR (r = 0.583), persisting after adjustment. In contrast, EH patients showed only weak correlations between PAC and eGFR (r = -0.204, p < 0.001), without links with other markers. Interaction analysis confirmed stronger PAC-biomarker associations in PA than EH (all p < 0.05). This study is the first to demonstrate robust associations between PAC and sensitive early renal damage biomarkers, especially RBP, in PA patients, distinct from matched EH patients. It highlights hyperaldosteronism's unique pathogenic role in renal impairment in PA, suggesting early biomarker monitoring and aldosterone-targeted interventions could reduce chronic kidney disease risk in PA populations.
原发性醛固酮增多症（PA）独立增加肾功能损害风险，超出血压影响范围。虽然已知醛固酮增多症介导肾损伤，但血浆醛固酮浓度（PAC）与视黄醇结合蛋白（RBP）和β2微球蛋白（β2-MG）等早期肾损伤生物标志物之间的关联仍未得到充分研究。我们调查了PAC与肾功能指标（包括RBP、β2-MG、白蛋白与肌酐比值（ACR）和估计肾小球滤过率（eGFR））之间的关联，比较了匹配的PA患者和原发性高血压（EH）患者。在这项横断面研究中，评估了546例PA患者和546例倾向评分匹配的EH患者。采用Spearman相关性分析和多变量回归分析评估PAC与肾脏标志物之间的关联，并进行交互作用检验以确定PA组和EH组之间的差异。在PA患者中，PAC与较低的eGFR（r = -0.597，p < 0.001）以及较高的RBP（r = 0.559）、β2-MG（r = 0.632）和ACR（r = 0.583）密切相关，调整后依然存在。相比之下，EH患者中PAC与eGFR之间仅显示出微弱的相关性（r = -0.204，p < 0.001），与其他标志物无关联。交互作用分析证实，PA患者中PAC与生物标志物之间的关联比EH患者更强（所有p < 0.05）。本研究首次证明了PA患者中PAC与敏感的早期肾损伤生物标志物（尤其是RBP）之间存在密切关联，这与匹配的EH患者不同。该研究突出了醛固酮增多症在PA患者肾功能损害中的独特致病作用，表明早期生物标志物监测和针对醛固酮的干预措施可能降低PA人群患慢性肾脏病的风险。
