Therefore, as an excellent fluorescence contrast agent, DIPT-ICF NPs can be applied to rapidly assess the reperfusion and function of renal grafts by monitoring NIR-II fluorescence on the surface of the kidney and in the urine. With the warm ischemia time increasing, the microvascular network in the glomerulus became degeneration and pyknosis, accompanied by the renal tubular epithelial cells degenerated and necrotic. (F) TEM images of the glomerular filtration barrier, of which the tissue was taken from the donor's kidneys undergoing warm ischemia times in (A), respectively. As the warm ischemia time increased, the damage to the three-layer structure of the glomerular basement membrane (GBM) was gradually aggravated, the foot process fusion of podocytes became more and more apparent, and the glomerular electron-dense layers became thinner and thinner. (G) Quantification of NIR-II mean intensity of the urine excreted from the ureters when the contrast agent DIPT-ICF NPs was infused into the donor rabbits' kidneys via the renal artery. The inset shows NIR-II images of the urine excreted from the ureters during perfusion of DIPT-ICF NPs in donor rabbits' kidneys undergoing warm ischemia in (A). The black and blue arrows in (D) and (E) represented atrophied glomerulus and degenerated necrotic tubules due to warm ischemia, respectively; the red and yellow arrows in (F) indicate GBM rupture and glomerular epithelial cell foot process fusion, respectively. All NIR-II images were captured under a 980 nm laser (60 mW/cm 2 ) with a 1319 nm LP and an exposure time of 200 ms.