However, as shown in Fig. , the change of the kidneys undergoing different degrees of warm ischemia could not be identified with the naked eyes. With the help of NIR-II fluorescence angiography technology, the discrepancies of kidneys upon different ischemia times could be rapidly identified (Fig. ). In general, normal kidney without ischemic injury showed uniformed fluorescence over the whole kidney after the injection of DIPT-ICF NPs from renal artery, while the fluorescence signal of the injured kidneys changed from uniformity to miliary distribution and show a decrease with different warm ischemia times (WITs) (Fig. and). Periodic Acid-Schiff (PAS) staining results indicated that in warm ischemia kidney models, the glomeruli volume decreased, accompanied by enlarged glomerular capsules and the corresponding renal tubular epithelial cells vacuolized, suggesting the lesion and necrosis of glomeruli and renal tubule (Fig. ). The ematoxylin and eosin (H&E) staining displayed that red blood cell trapping and congestion in renal microcirculation became more and more severe with the ischemia time, which induced the formation of microthrombus and caused the speckled distribution of fluorescence in the kidney (Fig. ). Additionally, the DIPT-ICF NPs were unable to pass through the glomerular filtration barrier (GFB) of normal kidneys (particle size of > 6 nm could not penetrate the GFB) , and were mainly excreted into the gut through the bile (Fig. ), appearing in the feces (Fig. ) rather than the urine (Fig. ). As shown in the TEM images (Fig. ), the three layers of glomerular filtration barrier (GFB) including the glomerular endothelial cell (GEC), glomerular basement membrane (GBM), and podocyte foot processes were damaged when suffering warm ischemia, which lead to DIPT-ICF NPs crossing through the GFB and entering the urine (Fig. ); thus, it is easily to identify GFB damages by urine fluorescence monitoring (Fig. ).