Elevated Exposure to Air Pollutants Accelerates Primary Glomerular Disease Progression

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 cen...

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Published in:Kidney international reports 2024-08, Vol.9 (8), p.2527-2536
Main Authors: 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
Format: Article
Language:English
Subjects:
black carbon
exposures
kidneys
PM2.5
progression
sulfates
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Summary: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 (PM2.5) 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. PM2.5, BC, and sulfate exposures were comparable in NEPTUNE (n = 228) and CureGN (n = 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 PM2.5 (adjusted hazard ratio 1.55 [95% confidence interval: 1.00–2.38], P = 0.0489) and BC (adjusted hazard ratio 1.43 [95% confidence interval: 0.98–2.07], P = 0.0608) exposure. Sulfate and PM2.5 exposure were positively correlated with serum tumour necrosis factor (TNF) (P = 0.003) and interleukin-1β levels (P = 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, P-value 
ISSN:2468-0249
2468-0249
DOI:10.1016/j.ekir.2024.05.013