Short-term gaseous and particulate air pollution exposure and risk of acute kidney injury: a 12-year case-crossover study [2013-2024] in Guangzhou, China.

BACKGROUND

Acute kidney injury (AKI) is a major public health burden associated with high morbidity, significantly increasing long-term mortality, and escalating healthcare costs. While long-term air pollution exposure is a known risk factor for chronic kidney disease (CKD), evidence regarding the acute triggers of AKI remains limited, especially in Asian megacities with complex pollution profiles. We investigated the independent effects of major air pollutants on the risk of AKI using algorithmically identified clinical data.

METHODS

A time-stratified case-crossover study was conducted involving adults in Guangzhou, China [2013-2024]. We included patients with longitudinal serum creatinine records and strictly excluded those with end-stage renal disease (ESRD) or a history of kidney transplantation. AKI events were defined using the Kidney Disease: Improving Global Outcomes (KDIGO) serum creatinine criteria. Daily meteorological and air pollutant data were collected from respective monitoring stations. Conditional logistic regression and generalized additive models were employed to estimate the associations between short-term exposure to fine particulate matter [particulate matter less than 2.5 μm (PM2.5)], sulfur dioxide (SO2), and nitrogen dioxide (NO2) and the risk of AKI, adjusting for meteorological factors.

RESULTS

A total of 10,857 AKI cases (60.0% male; 62.2% aged <65 years) were included. In multi-pollutant models, gaseous pollutants showed robust independent associations with AKI. A 10 µg/m3 increase in SO2 and NO2 was associated with a 4.6% [odds ratio (OR) =1.046, 95% confidence interval (CI): 1.027-1.066] and 3.3% (OR =1.033, 95% CI: 1.028-1.039) increase in AKI odds, respectively. NO2 showed immediate effects (lag 0), while SO2 exhibited delayed effects (lag 1). Notably, associations for NO2 and SO2 were significantly enhanced during the cold season. After adjusting for gaseous pollutants, PM2.5 exhibited a negative association (OR =0.977), which likely reflects statistical artifact due to high correlation rather than a protective biological effect.

CONCLUSIONS

Short-term exposure to ambient SO2 and NO2 are significant, independent risk factors for AKI in Guangzhou. These findings underscore the dominant nephrotoxic potential of gaseous pollutants. Clinicians should maintain heightened awareness of AKI risks during high-pollution episodes, particularly in the cold season, and multi-pollutant management strategies should be prioritized.