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Ultrastruct Pathol. 2018 Sep-Oct;42(5):430-439. doi: 10.1080/01913123.2018.1501125. Epub 2018 Oct 4.

Focal and segmental glomerulosclerosis in murine models: a histological and ultrastructural characterization with immunohistochemistry correlation of glomerular CD44 and WT1 expression.

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a Department of Pathology , College of Medicine, King Saud University , Riyadh , Saudi Arabia.
b Department of Family and Community Medicine , College of Medicine, University of Hail , Hail , Saudi Arabia.
c Department of Physiology , College of Medicine, University of Hail , Hail , Saudi Arabia.
d Department of Pharmacology , College of Medicine, King Saud University , Riyadh , Saudi Arabia.
e Intern , College of Medicine, King Faisal University , Riyadh , Saudi Arabia.
f Department of Medicine and Nephrology , College of Medicine, King Saud University , Riyadh , Saudi Arabia.



Focal segmental glomerulosclerosis (FSGS) is a common progressive chronic renal disease. Podocyte injury and loss are the postulated pivotal events that trigger FSGS. In this study, the authors aim to examine the evolution of FSGS in murine models histologically, ultrastructurally and immunohistochemically with special emphasis on podocytes and parietal epithelial cells (PECs).


FSGS resembling primary FSGS in humans was initiated in Wistar rats using intravenous Adriamycin injections. Blood and urine analysis were performed at 0, 8, and 12 weeks. Both the control kidneys and the test kidneys were harvested at 8 and 12 weeks, examined histologically and ultrastructurally and the findings correlated with the glomerular expression of immunostains specific for podocytes (WT-1) and for activated PECs (CD44).


FSGS developed in both 8 and 12 weeks test groups showing progressive proteinuria, podocytopathy and segmental glomerular scarring. There was a decrease in the glomerular expression of WT-1 with a concurrent increase in the glomerular expression of CD44, indicating podocyte loss with synchronous increase in activated PECs. The evolving FSGS correlated negatively with podocytes and positively with activated PECs.


Our study shows that with podocyte injury there is podocyte effacement and loss, proteinuria, glomerular segmental adhesion and scarring, all culminating in FSGS. In addition, there is activation, hyperplasia and hypertrophy of PECs. This demonstrates that both podocyte loss and PEC activation promote FSGS. Our findings are consistent with recent investigations. More studies are required to further understand the role of these cells in the evolution of FSGS and subsequently introduce new targeted treatment modalities.


Electron microscopy; Focal segmental glomerulosclerosis; immunohistochemistry CD44 and WT-1; parietal epithelial cells; podocytes

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