Air pollution and disease progression among patients with primary glomerular disease: an expanded study with extended follow-up

Background: Air pollution is increasingly recognized as a risk factor for progression of kidney disease; however, few studies have examined its impact among patients with primary glomerular disorders. To address this knowledge gap, we previously reported positive associations between fine particulate matter ≤ 2.5μm in aerodynamic diameter (PM_2.5) and black carbon with kidney disease progression in an observational cohort of children and adults (n = 925) with primary glomerular diseases, namely minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, and IgA nephropathy. In the current study, we leverage the same cohort to (1) identify additional air pollutants that may be associated with kidney disease progression using data from the National Center for Atmospheric Research (NCAR); (2) determine whether the association between baseline air pollution exposure and kidney disease progression is maintained over a longer follow-up period; and (3) assess whether associations identified in our previously published findings remain when using NCAR pollutant data. Methods: In this retrospective cohort study, we obtained air pollutant concentration data from NCAR based on participant residential census tract at enrollment. For each census tract and pollutant, we aggregated daily pollutant concentrations to annual averages. We used Cox proportional hazards models to estimate associations between average baseline pollutant exposure and time to kidney disease progression, defined as a 40% decline in estimated glomerular filtration rate (eGFR) or occurrence of kidney failure (eGFR) < 15 ml/min/1.73 m²) during follow-up. Hazard ratios (HR) represented a doubling of exposure. Results: Use of NCAR data supported our previous findings of adverse effects of PM_2.5 and black carbon on the progression of glomerular disease. Moreover, using the NCAR data we identified novel associations with NO₂ exposure, HR 1.12 [1.01, 1.26] and specific components of PM_2.5, including organic matter, HR 1.17 [1.01, 1.37] and an increased risk of disease progression. When considering a longer follow-up period, associations between baseline exposures and kidney outcomes persisted, but were attenuated suggesting a need for recent, interval-specific risk assessment, inclusion of acute exposures, and enhanced spatial resolution of exposures. Conclusion: Our findings highlight the importance of the systematic assessment including spatial and temporal variation of a broad range of air pollution components to determine the impact of exposure on short- and long-term outcomes in patients with primary glomerular disease (word count: 368).