Expression of Alpha Smooth Muscle Actin and Lysozyme in Various Glomerular Diseases.
- Author:
Sun Hee SUNG
;
Woon Sup HAN
- Publication Type:Original Article
- Keywords:
Glomerular disease;
Alpha-smooth muscle actin;
Lysozyme;
Microfilament;
Mesangium
- MeSH:
Actin Cytoskeleton;
Actins*;
Biopsy;
Diagnosis;
Disease Progression;
Glomerular Mesangium;
Glomerulonephritis;
Glomerulonephritis, IGA;
Glomerulonephritis, Membranoproliferative;
Glomerulonephritis, Membranous;
Glomerulosclerosis, Focal Segmental;
Humans;
Kidney;
Macrophages;
Mesangial Cells;
Muramidase*;
Muscle, Smooth*;
Nephrosis, Lipoid;
Sclerosis
- From:Korean Journal of Pathology
1998;32(1):51-57
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The cells of glomerular mesangium is composed mostly of intrinsic contractile mesangial cells and a few macrophages. Injury to the mesangium is central to many glomerular diseases. This study was aimed to evaluate and compare the expressions of alpha-smooth muscle actin (ASMA) and lysozyme in the mesangium of various human glomerular diseases and also of according to the severity of their progressions. We performed immunohistochemical and transmission electromicroscopic examinations in 51 cases of renal biopsy including 5 normal kidneys. The results were as follows; (1) ASMA staining was negligible in normal glomeruli. (2) Increased ASMA staining was observed in the mesangium of glomeruli from all specimens of primary glomerular disease, regardless of their diagnosis. (3) The staining intensity of ASMA in mesangium was mild in minimal change disease and membranous glomerulonephritis, and strong in focal segmental glomerulosclerosis (FSGS), diffuse mesangial hypercellularity, membranoproliferative glomerulonephritis (MPGN), and IgA nephropathy (IgAN). (4) The staining intensity of ASMA have no correlation with mesangial immune deposits. (5) The staining intensity of ASMA in mesangium was inversely correlated with the disease progression in FSGS and IgAN. (6) Glomeruli showing global or segmental sclerosis invariably lacked ASMA. (7) Compared with ASMA, the mesangial cells with lysozyme expression were very rare, even though it was in proportion to ASMA staining. Interstitial ASMA expression was confined to fibrotic area in various glomerular diseases. In conclusion, the expression of ASMA and lysozyme in mesangium are increased in a variety of glomerular diseases, regardless of disease entity. Their intensity was in proportion to the mesangial cell proliferation. In progressive glomerulonephritis, such as IgAN and FSGS, the increased expression of ASMA was prominent in the early lesion, and decreased with the progression of the glomerular sclerosis.
