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Published on: August 19, 2020
Elevated Exposure to Air Pollutants Accelerates Primary Glomerular Disease Progression
Jonathan P Troost1, Jennifer D'Souza2, Miatta Buxton2
1Michigan Institute for Clinical & Health Research, University of Michigan, Ann Arbor Michigan, USA.
Air pollution, specifically fine particulate matter (PM2.5) and black carbon (BC), accelerates kidney disease progression in patients with primary glomerulopathies. Exposure to these pollutants also correlates with increased systemic inflammation markers.
Area of Science:
- Nephrology
- Environmental Health
- Epidemiology
Background:
- Environmental factors contributing to kidney disease progression are not fully understood.
- Primary glomerulopathies represent a significant cause of kidney disease.
Purpose of the Study:
- To investigate the association between residential air pollution exposure and kidney disease progression in patients with primary glomerulopathies.
- To explore potential molecular mechanisms linking air pollution to kidney disease progression.
Main Methods:
- Utilized data from the Nephrotic Syndrome Study Network (NEPTUNE) and CureGlomerulonephropathy (CureGN) cohorts.
- Employed Cox proportional hazards models to assess the impact of PM2.5, black carbon (BC), and sulfate exposure on kidney disease progression (≥40% eGFR decline or kidney failure).
- Measured serum tumor necrosis factor (TNF) and kidney tissue transcriptomic inflammatory pathway activation as biomarkers.
Main Results:
- Higher PM2.5 and BC exposure were associated with increased risk of kidney disease progression in a combined analysis of both cohorts.
- Sulfate and PM2.5 exposure correlated with elevated serum TNF and interleukin-1β levels.
- Sulfate exposure was linked to the activation of TNF and JAK-STAT signaling pathways in kidney tissue.
Conclusions:
- Elevated exposure to PM2.5 and BC is linked to accelerated kidney disease progression in primary glomerulopathies.
- Air pollution exposure may promote kidney disease progression through systemic inflammation and activation of inflammatory pathways.
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