Objective To investigate the influence of chronic renal disease (CKD) on acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and hospitalization.Methods Fifty patients clinically diagnosed as COPD complicating CKD in our hospital from January 2011 to June 2013 were selected as the observation group and 50 patients with CKD-free COPD were taken as a control group.The comparative analysis was performed by retrospecting the data of lung function,exercise tolerance and hospitalization situation in 1 year follow up.Results The mortality rate,total occurrence rate of AECOPD,occurrence rate of severe AECOPD,hospitalization rate,hospitalization time,self-rating test (CAT) score,mMRC dyspnea index,CRP and blood creatinine level in the observation group were higher than those in the control group,the difference was statistically significant (P<0.05);FEV1%pred,6MWD and creatinine clearance rate in the observation group were lower than those in the control group,the difference was statistically significant (P<0.05);FEV1/FVC had no statistical difference between the two groups (P>0.05).Conclusion The condition in COPD patients complicating CKD at 1 year after clinical diagnosis is significantly aggravated compared with COPD patients without complicating CKD,and the prognosis for patients complicated with CKD is poorer.

Silicosis is a leading cause of occupational disease-related morbidity and mortality worldwide, but the molecular basis underlying its development remains unclear. An accumulating body of evidence supports gasdermin D (GSDMD)-mediated pyroptosis as a key component in the development of various pulmonary diseases. However, there is little experimental evidence connecting silicosis and GSDMD-driven pyroptosis. In this work, we investigated the role of GSDMD-mediated pyroptosis in silicosis. Single-cell RNA sequencing of healthy and silicosis human and murine lung tissues indicated that GSDMD-induced pyroptosis in macrophages was relevant to silicosis progression. Through microscopy we then observed morphological alterations of pyroptosis in macrophages treated with silica. Measurement of interleukin-1β release, lactic dehydrogenase activity, and real-time propidium iodide staining further revealed that silica induced pyroptosis of macrophages. Additionally, we verified that both canonical (caspase-1-mediated) and non-canonical (caspase-4/5/11-mediated) signaling pathways mediated silica-induced pyroptosis activation, in vivo and in vitro. Notably, Gsdmd knockout mice exhibited dramatically alleviated silicosis phenotypes, which highlighted the pivotal role of pyroptosis in this disease. Taken together, our results demonstrated that macrophages underwent GSDMD-dependent pyroptosis in silicosis and inhibition of this process could serve as a viable clinical strategy for mitigating silicosis.