Wistrand Henrik, Kaartinen Niina E, Jousilahti Pekka, Jalkanen Sirpa, Salmi Marko, Niiranen Teemu, Langén Ville Lauri
Faculty of Medicine, University of Turku, Turku, Finland.
Division of Medicine, Turku University Hospital and University of Turku, Turku, Finland.
Integr Blood Press Control. 2024 Dec 12;17:51-57. doi: 10.2147/IBPC.S483495. eCollection 2024.
The complex pathogenesis of hypertension, potentially involving inflammatory pathways, remains elusive. This study aimed to evaluate the relationship between 24-hour urinary sodium excretion and inflammatory cytokines alongside C-reactive protein (CRP) in a nationwide Finnish sample.
265 participants from the FINRISK 2002 study were included in the analyses. Multivariable-adjusted associations of 24-hour urinary sodium with circulating CRP and 26 cytokines were examined.
24-hour urinary sodium was not significantly associated with any of the cytokines or CRP (p ≥ 0.02 for all, significance at <0.001). Adjustments for age, sex, serum creatinine concentration, and alcohol intake did not alter these results.
This cross-sectional study revealed no associations between 24-hour urinary sodium and cytokine or CRP levels. This does not suggest reducing salt intake would be unbeneficial in hypertension. Additional research is required to clarify the mechanisms through which salt may induce hypertension. Assessing sodium intake in epidemiological studies is also challenging.
高血压的发病机制复杂，可能涉及炎症途径，但仍不清楚。本研究旨在评估芬兰全国样本中24小时尿钠排泄与炎症细胞因子以及C反应蛋白（CRP）之间的关系。
分析纳入了来自2002年芬兰全国心血管疾病风险因素研究（FINRISK 2002）的265名参与者。研究了24小时尿钠与循环CRP及26种细胞因子的多变量调整关联。
24小时尿钠与任何细胞因子或CRP均无显著关联（所有p≥0.02，显著性水平<0.001）。对年龄、性别、血清肌酐浓度和酒精摄入量进行调整后，这些结果未改变。
这项横断面研究显示24小时尿钠与细胞因子或CRP水平之间无关联。这并不意味着减少盐摄入量对高血压患者没有益处。需要进一步研究以阐明盐可能诱发高血压的机制。在流行病学研究中评估钠摄入量也具有挑战性。
