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Updated: Jun 6, 2026

Imaging of Podocytic Proteins Nephrin, Actin, and Podocin with Expansion Microscopy
Published on: April 23, 2021
Immunohistochemical evaluation of podocalyxin expression in glomerulopathies associated with nephrotic syndrome
Evangelia Kavoura1, Hariklia Gakiopoulou, Helen Paraskevakou
1First Department of Pathology, School of Medicine, National and Kapodistrian University of Athens, Athens 11527, Greece.
Abstract:
It is now well established that morphological change of podocytes is closely correlated to the development of proteinuria. The aim of this study was to investigate the role of podocalyxin, a major podocyte protein, in the pathogenesis of glomerulopathies primarily associated with the nephrotic syndrome. Immunohistochemical expression of podocalyxin has been evaluated in 51 renal samples, including healthy controls, patients with podocytopathies (minimal change disease [MCD], focal segmental glomerulosclerosis [FSGS]) and membranous glomerulopathy (MG). A computerized image analysis program has been used. Statistical analysis was performed using analysis of variance and Bonferroni tests. Immunohistochemical expression of podocalyxin has been observed within the podocytes of healthy controls. In MCD, podocalyxin expression was globally reduced despite the normal appearance of the glomeruli. In FSGS, podocalyxin loss was observed in both the segmental sclerotic and the nonsclerotic areas being significantly more prominent in the former. Reduction of podocalyxin in MG was demonstrated for the first time immunohistochemically. The percentage of the stained area was statistical significantly higher in the controls than in each pathologic group. However, among pathologic groups (FSGS, MCD, MG), there was no statistically significant difference. This is one of the few studies investigating podocalyxin immunohistochemical expression in glomerulopathies associated with nephrotic syndrome. The observed reduction in podocalyxin expression suggests that it constitutes a target molecule in nephrotic syndrome pathogenesis regardless of the underlying cause.
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