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. Author manuscript; available in PMC: 2022 Feb 8.
Published in final edited form as: Kidney Int. 2020 Sep 8;99(1):173–185. doi: 10.1016/j.kint.2020.08.021

Figure 3 |. Histological characteristics of the transition from acute kidney injury (AKI) to chronic kidney disease (CKD).

Figure 3 |

(a,b) Representative tubular dilation in AKI group compared with the controls, where areas of tubular dilation were frequent in the AKI group (b; red *). (c) The quantification of the percentage of white space. Scarred area (d–f) was assessed by trichrome stain in the CKD-4 and CKD-12 groups. (e) The kidneys in the CKD-4 and CKD-12 groups were smaller and had cortical wedge-shaped lesions. These scarred areas contained many atrophic tubules and lotus-negative glomeruli (h). (g–i) Lotus-negative glomeruli and (j–l) proximal tubular fraction were assessed on lotus lectin stained kidneys. (g) A healthy glomerulus in a control animal where the glomerulus is connected to the tubule. The red arrows highlight the parietal cells marked as lotus-positive signifying an intact glomerulotubular junction. (j–l) Proximal tubular content was reduced in the CKD-12 group. Bars in the histologic sections = 50 μm. P values < 0.002 are considered significant. CKD-4, CKD 4 weeks after injury; CKD-12, CKD 12 weeks after injury. To optimize viewing of this image, please see the online version of this article at www.kidney-international.org.