nitrogen-dioxide and Kidney-Diseases

Long-term exposure to air pollution has been associated with the onset and progression of kidney diseases, but the association between short-term exposure to air pollution and mortality of kidney diseases has not yet been reported.. A nationally representative sample of 101,919 deaths from kidney diseases was collected from the Chinese Center for Disease Control and Prevention from 2015 to 2019. A time-stratified case-crossover study was applied to determine the associations. Satellite-based estimates of air pollution were assigned to each case and control day using a bilinear interpolation approach and geo-coded residential addresses. Conditional logistic regression models were constructed to estimate the associations adjusting for nonlinear splines of temperature and relative humidity.. Each 10 µg/m

Topics: Air Pollutants; Air Pollution; China; Cross-Over Studies; Humans; Kidney Diseases; Nitrogen Dioxide; Particulate Matter

Several studies have shown that long-term exposure to air pollution is associated with reduced kidney function. However, less is known about effects of short-term exposure to air pollution on kidney disease aggravation and resultant emergency room (ER) burden. This study aimed to estimate excess ER visits attributable to short-term air pollution and to provide evidence relevant to air pollution standards to protect kidney patients.. We conducted time-series analysis using National Health Insurance data covering all persons in South Korea (2003-2013). We collected daily data for air pollutants (particulate matter ≤10 µm [PM10], ozone [O3], carbon monoxide [CO], and sulfur dioxide [SO2]) and ER visits for total kidney and urinary system disease, acute kidney injury (AKI), and chronic kidney disease (CKD). We performed a two-stage time-series analysis to estimate excess ER visits attributable to air pollution by first calculating estimates for each of 16 regions, and then generating an overall estimate.. For all kidney and urinary disease (902,043 cases), excess ER visits attributable to air pollution existed for all pollutants studied. For AKI (76,330 cases), we estimated the highest impact on excess ER visits from O3, while for CKD (210,929 cases), the impacts of CO and SO2 were the highest. The associations between air pollution and kidney ER visits existed for days with air pollution concentrations below current World Health Organization guidelines.. This study provides quantitative estimates of ER burdens attributable to air pollution. Results are consistent with the hypothesis that stricter air quality standards benefit kidney patients.

Topics: Air Pollutants; Air Pollution; Humans; Kidney Diseases; Nitrogen Dioxide; Ozone; Particulate Matter; Sulfur Dioxide

Chronic nitric oxide synthase inhibition (NOSI) causes chronic kidney disease (CKD) in the Sprague Dawley (SD) rat. We previously showed that the Wistar-Furth (WF) rats are resistant to several models of CKD and maintain renal nitric oxide (NO) production compared with SD rats, whereas low-dose NOSI caused progression of CKD in WF rats. Here, we evaluate the impact of high-dose chronic NOSI in WF and SD rats, as well as intrarenal responses to an acute pressor dose of NOSI in the normal WF. Rats were given N(G)-nitro-l-arginine methyl ester (l-NAME) (150 and 300 mg/l for 6-10 wk) in the drinking water after an initial bolus tail vein injection. Both strains showed significant reductions in total NO production with chronic l-NAME. SD given 150 mg/l l-NAME for 6 wk developed proteinuria and renal injury, whereas WF rats receiving 150 mg/l l-NAME for 6-10 wk or 300 mg/l for 6 wk developed no proteinuria and minimal renal injury. Blood pressure was significantly elevated with chronic NOSI in both strains but was higher in the SD rat. There was little impact on renal nitric oxide synthase expression with l-NAME, except that cortical endothelial nitric oxide synthase abundance increased in WF after 6 wk (150 mg/l). Micropuncture experiments with acute pressor NOSI resulted in similar increases in systemic blood pressure in SD and WF rats, whereas WF rats showed a much smaller increment in glomerular blood pressure compared with SD rats. In conclusion, WF rats do not develop renal injury after chronic NOSI at, or above, a dose that causes significant injury in the SD rat. This protection may be associated with protection from glomerular hypertension.

Topics: Animals; Chronic Disease; Dose-Response Relationship, Drug; Kidney; Kidney Diseases; NG-Nitroarginine Methyl Ester; Nitric Oxide Synthase; Nitrogen Dioxide; omega-N-Methylarginine; Puromycin; Rats; Rats, Inbred WF; Rats, Sprague-Dawley; Time Factors