NLRP3 and IgA glomerulonephritis: Accumulating preclinical and clinical evidence in recent years demonstrates that aberrant activation of the NLRP3 inflammasome directly promotes glomerular damage, tubulointerstitial inflammation, fibrosis, and vascular dysfunction through the release of IL-1β and IL-18 and the induction of pyroptosis, thereby contributing to the pathogenesis of diverse renal disorders including acute kidney injury (AKI), diabetic kidney disease (DKD), IgA nephropathy, lupus nephritis, and chronic renal fibrosis.