Troost Jonathan P, D'Souza Jennifer, Buxton Miatta, Kshirsagar Abhijit V, Engel Lawrence S, O'Lenick Cassandra R, Smoyer William E, Klein Jon, Ju Wenjun, Eddy Sean, Helmuth Margaret, Mariani Laura H, Kretzler Matthias, Trachtman Howard
Michigan Institute for Clinical & Health Research, University of Michigan, Ann Arbor Michigan, USA.
Department of Epidemiology, University of Michigan, Ann Arbor, Michigan, USA.
Kidney Int Rep. 2024 May 18;9(8):2527-2536. doi: 10.1016/j.ekir.2024.05.013. eCollection 2024 Aug.
Environmental contributors to kidney disease progression remain elusive. We explored how residential air pollution affects disease progression in patients with primary glomerulopathies.
Nephrotic Syndrome Study Network (NEPTUNE) and CureGlomerulonephropathy (CureGN) participants with residential census tract data and ≥2 years of follow-up were included. Using Cox proportional hazards models, the associations per doubling in annual average baseline concentrations of total particulate matter with diameter ≤2.5 μm (PM) and its components, black carbon (BC), and sulfate, with time to ≥40% decline in estimated glomerular filtration rate (eGFR) or kidney failure were estimated. Serum tumour necrosis factor levels and kidney tissue transcriptomic inflammatory pathway activation scores were used as molecular markers of disease progression.
PM, BC, and sulfate exposures were comparable in NEPTUNE ( = 228) and CureGN ( = 697). In both cohorts, participants from areas with higher levels of pollutants had lower eGFR, were older and more likely self-reported racial and ethnic minorities. In a fully adjusted model combining both cohorts, kidney disease progression was associated with PM (adjusted hazard ratio 1.55 [95% confidence interval: 1.00-2.38], = 0.0489) and BC (adjusted hazard ratio 1.43 [95% confidence interval: 0.98-2.07], = 0.0608) exposure. Sulfate and PM exposure were positively correlated with serum tumour necrosis factor (TNF) ( = 0.003) and interleukin-1β levels ( = 0.03), respectively. Sulfate exposure was also directly associated with transcriptional activation of the TNF and JAK-STAT signaling pathways in kidneys (r = 0.55-0.67, -value <0.01).
Elevated exposure to select air pollutants is associated with increased risk of disease progression and systemic inflammation in patients with primary.
导致肾病进展的环境因素仍不明确。我们探讨了居住空气污染如何影响原发性肾小球疾病患者的疾病进展。
纳入肾病综合征研究网络（NEPTUNE）和治愈肾小球肾炎（CureGN）中具有居住普查区数据且随访时间≥2年的参与者。使用Cox比例风险模型，估计直径≤2.5μm的总颗粒物（PM）及其成分黑碳（BC）和硫酸盐的年平均基线浓度每增加一倍与估计肾小球滤过率（eGFR）下降≥40%或肾衰竭时间之间的关联。血清肿瘤坏死因子水平和肾组织转录组炎症途径激活评分用作疾病进展的分子标志物。
NEPTUNE（n = 228）和CureGN（n = 697）中的PM、BC和硫酸盐暴露情况相当。在两个队列中，来自污染物水平较高地区的参与者eGFR较低，年龄较大，且更有可能自我报告为种族和族裔少数群体。在结合两个队列的完全调整模型中，肾病进展与PM（调整后风险比1.55 [95%置信区间：1.00 - 2.38]，P = 0.0489）和BC（调整后风险比1.43 [95%置信区间：0.98 - 2.07]，P = 0.0608）暴露相关。硫酸盐和PM暴露分别与血清肿瘤坏死因子（TNF）（P = 0.003）和白细胞介素 - 1β水平（P = 0.03）呈正相关。硫酸盐暴露还与肾脏中TNF和JAK - STAT信号通路的转录激活直接相关（r = 0.55 - 0.67，P值<0.01）。
接触特定空气污染物水平升高与原发性患者疾病进展风险增加和全身炎症相关。
