Altered Expression of Nephrin, Glomerular Epithelial Cell Protein-1 (GLEPP1) and WT-1 in Glomerular Disease.
- Author:
Byoung Kwon KIM
1
;
Ji Hoon KIM
;
Hyun Soon LEE
Author Information
1. Department of Pathology, Seoul National University College of Medicine, Seoul 110-744, Korea. Hyunsoon@plaza.snu.ac.kr
- Publication Type:Original Article
- Keywords:
Nephrosis-Lipoid-Glomerulo Nephritis-Biological Markers
- MeSH:
Biomarkers;
Biopsy;
Diaphragm;
Epithelial Cells*;
Female;
Filtration;
Glomerulosclerosis, Focal Segmental;
Humans;
Male;
Nephrectomy;
Nephritis;
Nephrosis, Lipoid;
Proteinuria
- From:Korean Journal of Pathology
2002;36(1):21-29
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Glomerular epithelial cell protein-1 (GLEPP1) and WT-1 expressed in mature visceral glomerular epithelial cell (VGEC) is required for maintenance of the mature status of VGEC. Nephrin protein is located at the filtration slit and regarded as a molecular component of the slit diaphragm. Alterations of these proteins in proteinuric diseases are not clearly defined. METHODS: We investigated the expression of GLEPP1, WT-1 and nephrin in 28 renal biopsies diagnosed with minimal change nephropathy (n=10), focal glomerulosclerosis (n=10) and membranous nephritis (n=8) by immunohistochemical staining. Normal control biopsies were obtained from six nephrectomy specimens. RESULTS: The patients consisted of 15 males and 13 females. The mean age was 40.7 years. Nephrotic range proteinuria (> or =3.5 g/day) was noted in 15 (54%) patients. GLEPP1 and nephrin expression were significantly decreased in patients as compared with those of the controls (p<0.05). The mean number of WT-1 expressing cells per glomerulus was also significantly decreased in patients as compared with those of the controls (p<0.05). However, there was no significant difference in the number of WT-1 expressing cells among the disease groups. CONCLUSIONS: These results suggest that the loss of biological markers of mature VGEC may play an important role in the pathogenesis of proteinuria.
