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Original Articles
- Expression of Alpha Smooth Muscle Actin and Lysozyme in Various Glomerular Diseases.
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Sun Hee Sung, Woon Sup Han
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Korean J Pathol. 1998;32(1):51-57.
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Abstract
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- 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.
- Image Analysis of Glomerular Changes in Patients with Post-transplant IgA Nephropathy.
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Kye Won Kwon, Hyeon Joo Jeong
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Korean J Pathol. 2001;35(3):206-211.
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Abstract
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- BACKGROUND
IgA nephropathy after renal transplantation (post-transplant IgAN) may recapitulate the IgAN of native kidneys, however, little has been reported about the histologic characteristics. The aim of this study is to apply glomerular morphometry using an image analyser to examine the histologic characteristics of post-transplant IgAN.
METHODS
The outer margin of the glomerulus (Bowman's area, BA) and glomerular tuft area (GA) were traced manually. The measured area were automatically calculated by KS300 image analysis system (Kontron, Munchen, Germany). The mesangial area (MA) was calculated with a summing each manually traced mesangial area. The total number of glomerular (GC) and mesangial cells (MC) were counted. Eight cases of renal section obtained by nephrectomy due to renal cell carcinoma (normal control: N-CTRL) and nineteen cases of renal section obtained from post-transplantation patients without IgAN (transplantation control: Tx-CTRL) served as controls.
RESULTS
A total of 35 biopsies were finally selected for measurement. BA and GA of post-transplant IgAN were 1.6 and 1.4 times larger than the N-CTRL, respectively, and were not significantly different from Tx-CTRL. MA was 1.4 times significantly larger than that of the Tx-CTRL. As compared to that of the N-CTRL, it was 1.2 times larger, but this difference was not statistically significant. The GC and MC of post-transplant IgAN and the Tx-CTRL were significantly lower than the N-CTRL. There were no significant correlations between glomerular hypertrophy and duration after renal transplantation, mesangial changes, segmental sclerosis, or degree of renal cortical interstitial fibrosis in post-transplant IgAN.
CONCLUSIONS
Prominent glomerular hypertrophy and mesangial expansion suggest a hyperfiltration injury in post-transplant IgAN and a possible way to glomerulosclerosis.
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