Autor: |
OOTAKA, Tetsuya, SATO, Hiroshi, ITO, Sadayoshi, SATO, Toshinobu, SAITO, Takao |
Jazyk: |
angličtina |
Rok vydání: |
2004 |
Předmět: |
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Zdroj: |
東北大学医学部保健学科紀要 = Bulletin of School of Health Sciences Tohoku University. 13(1):65-77 |
ISSN: |
1348-8899 |
Popis: |
To investigate the correlation of phenotypic change of mesangial cells and injury of podocytes in the progression of IgA nephropathy, we performed a longitudinal study on 38 patients who underwent repeated renal biopsies. The patients were subdivided into two groups according to the clinical course between the initial and the follow-up bipsies : Group R (remission ; 20 cases) and Group P (progression ; 18 cases). The epithelial expression of CR1 and mesangial expression of α-smooth muscle actin (SMA), low-molecular weight caldesmon (L-CLD) and high-molecular weight caldesmon (H-CLD) was evaluated by immunoperoxidase method. The expression of these antigens was compared with the glomerular infiltration of macrophages and several histological and clinical parameters indicating glomerular injury. Also, the sequential changes in these parameters were evaluated in each group. The mesangial expression of SMA and L-CLD was observed in variable intensity and was significantly correlated with glomerular infiltration of macrophages, reduction of epithelial expression of CR1, mesangial expansion/cellularity and 24-hour urine protein. Both the expression of L-CLD and the reduction of CR1 were correlated with capsular adhesion. In the longitudinal analysis, persistent infiltration of macrophages was associated with persistent or increased expression of SMA/L-CLD, reduced expression of CR1, increased mesangial expansion and progression of glomerular sclerosis. These findings suggested that macrophages infiltrating in glomeruli might be involved in the induction or promotion of SMA and L-CLD expression and that these contractile proteins might be involved in the induction and progression of mesangial and epithelial injury in IgA nephropathy. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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