NETS in Renal disease

Neutrophils play a crucial role in the removal of microbes through various processes such as phagocytosis,ROS generation,degranulation,and the ejection of chromatin fibres containing antimicrobial peptides and enzymes.These structures render invading microbes immobile and can contribute to inflammatory and autoimmune diseases. Neutrophils release neutrophil extracellular traps (NETs) in response to infectious and sterile stimuli,which are independent of apoptosis.NETs activate plasmacytoid dendritic cells(pDCs)when they externalize granular peptides in combination with DNA. NETosis can be triggered by cytokines,complement activation factors,autoantigens,immunological complexes,and autoantibodies. NET peptides activate the NLRP3 inflammasome in macrophages,causing the production of IL-1 and IL-18. Aim of the work:The association between the degree of AKI and the expression of NETs. Material and Methods: The study involved 106 participants, including 33 healthy individuals, 73 patients (38 male,35 female,52.2%),and 33 non-abnormal individuals.A control group of 22 males and 11 females aged 18-90 years was selected from the intensive care unit. Results:A statistically significant difference was found when comparing the laboratory findings of the cases and control groups.The cases showed a significantly higher level of renal function (urea & creatinine) compared to the control group (p value <0.0001 & <0.0001 respectively),a significantly lower estimated glomerular filteration rate (p value <0.0001),and a significantly different level of neutrophil cytoplasmic traps (p value<0.0001). Conclusion:Neutrophils, innate immune cells, secrete cytokines and NETs, which promote inflammation and can cause glomerular injury, autoimmune processes, vascular damage, and kidney fibrosis.When NET creation is disrupted with clearance,kidneys suffer.Research suggests that NET-associated process modulation could be a potential treatment for numerous inflammatory kidney diseases.