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. Author manuscript; available in PMC: 2019 Oct 1.
Published in final edited form as: Matrix Biol. 2018 Apr 16;71-72:250–261. doi: 10.1016/j.matbio.2018.04.008

Fig. 3. Transmission electron microscopy demonstrates splitting and thickening of the GBM in the Col4a3−/− mouse model of Alport syndrome.

Fig. 3

A. Early stage of pathology shows mild GBM splitting and thickening (asterisk) with preserved podocyte foot processes (arrows) and endothelial cell fenestrations (arrowheads). B. Later stage of pathology shows extensive GBM splitting and thickening (black asterisk) and effacement of podocyte foot processes (arrows). Endothelial cell fenestrations appear to be maintained (arrowheads), and there is evidence of podocyte invasion into the GBM towards the endothelium (white asterisks). Some of these processes appear embedded in the GBM due to the plane of section.