Skip to main content
Fig. 1 | BMC Nephrology

Fig. 1

From: The role of podocyte damage in the etiology of ischemia-reperfusion acute kidney injury and post-injury fibrosis

Fig. 1

a: HE b: Masson Histology of kidneys on the 28th day after renal injury. AKI 20 group (mice underwent renal artery clamping for 20 min followed by contralateral nephrectomy 8 days after injury), AKI 30 group (mice underwent renal artery clamping for 30 min followed by contralateral nephrectomy 8 days after injury), AKI 40 groups (mice underwent renal artery clamping for 40 min followed by contralateral nephrectomy 8 days after injury). Kidneys were collected, and 3-mm paraffin sections were stained with hematoxylin and eosin (HE) stain and Masson’s trichrome. Scale bar =50 μm. Higher magnification: 1. Tumor tubular epithelial cells are swollen and the particles denote vacuolar degeneration. 2. Partial tubular epithelial cell damage with brush border detachment. Part of the renal tubular epithelial cells are necrotic. 3. Infiltration of renal interstitial lymphoid mononuclear cells. Renal tubular epithelial cells are swollen and the particles denote vacuolar degeneration. 4. Renal interstitial exchange for a small amount of lymphocyte mononuclear cell infiltration. 5. Renal interstitial infiltration of multiple lymphoid mononuclear cells with interstitial fibrosis. 6. Renal interstitial fibrosis, tubular atrophy

Back to article page