The PM2.5 component, benzo[b]fluoranthene, may contribute to the pathogenesis of membranous nephropathy by activating phosphoinositide 3-kinase/protein kinase B pathway and causing podocyte pyroptosis.

Membranous nephropathy (MN) is the main type of adult nephrotic syndrome, and its prevalence is increasing annually. An increasing number of studies have suggested that the pathogenesis of MN is related to 2.5-μm particulate matter (PM2.5), but the underlying mechanism has not been elucidated fully. Elucidating this mechanism can help prevent and treat MN. The constituents of PM2.5 vary from place to place; hence, the component responsible for PM2.5-related MN is still unclear. This study investigated the effects of benzo[b]fluoranthene (BbF), a PM2.5 component, on pyroptosis and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signalling pathway in Sprague-Dawley rats and mouse podocytes. The organic constituents of BbF in PM2.5 can enter the circulatory system through the lungs and act on the kidneys to cause kidney damage, possibly because BbF activates the PI3K/AKT pathway and causes podocytes to undergo pyroptosis.