PM_2.5 exposure is associated with a glomerular filtration rate (GFR) reduction, and renal tissue damage. The goal of this study was demonstrate the acute effect of PM_2.5 on the kidney. Male rats were acutely exposed to PM_2.5 or filtered air. Blood pressure was mesure and early kidney biomarkers were evaluated in serum and urine samples, and also IL-1β, IL-6 and TNFα were determined. Oxidative biomarkers, angiotensin/bradykinin-related proteins, KIM-1, IL-6 and histology were determined. Blood pressure, GFR, and early kidney damage biomarkers increase together with oxidative biomarkers and angiotensin/bradykinin endocrine-related proteins increased after exposure to PM_2.5. Urinary IL-6 increased after exposure to PM_2.5, whereas in kidney cortex decreased. Histological changes were observed and accompanied by the induction of KIM-1. Acute exposure to PM_2.5 not decline kidney function. However, it can induce early kidney damage biomarkers, oxidative stress, inflammation and angiotensin mediators, which perhabs culminates in a lose of renal function.

PM _2.5暴露与肾小球滤过率（GFR）降低和肾组织损害有关。这项研究的目的是证明PM _2.5对肾脏的急性作用。雄性大鼠急性暴露于PM _2.5或过滤空气中。可以测量血压，并在血清和尿液样品中评估早期肾脏生物标志物，还可以测定IL-1β，IL-6和TNFα。确定了氧化生物标志物，血管紧张素/缓激肽相关蛋白，KIM-1，IL-6和组织学。暴露于PM _2.5后，血压，GFR和早期肾脏损害生物标志物增加，而氧化生物标志物和血管紧张素/缓激肽内分泌相关蛋白增加。暴露于PM _2.5后尿液IL-6升高，而肾皮质减少。观察到组织学变化并伴随KIM-1的诱导。急性暴露于PM _2.5不会降低肾功能。但是，它可以诱导早期肾脏损伤的生物标志物，氧化应激，炎症和血管紧张素介体，这些可能最终导致肾功能丧失。