Gouty nephropathy is a common complication of gout, which is characterized pathologically by the abnormal deposition of urate crystals in the kidneys. This deposition can directly trigger local inflammatory responses and lead to renal tissue damage. Neutrophil extracellular traps (NETs), as a unique neutrophil-derived immune defense mechanism, play a key pro-inflammatory role in gouty nephropathy. Under conditions of long-term hyperuricemia, Monosodium urate (MSU) crystals can activate related inflammatory signaling pathways, promoting inflammatory cell infiltration, the release of pro-inflammatory factors, and the formation of NETs, thereby exacerbating inflammatory responses and fibrosis in hyperuricemic nephropathy. This review summarizes the formation and pro-inflammatory injury mechanisms of NETs in gouty nephropathy and discusses the potential and challenges of targeting NETs as a novel therapeutic strategy for gout-related kidney disease.
梁 et al. (Wed,) studied this question.