腎疾患における糸球体アクチンの動態

抄録

Actin is shown previously to be present in the glomeruli using Heavy meromyosin coupled with a fluorescent dye, N-(7-Dimethylamino-4-Methylcoumarinyl) Maleimide (DACM), Distribution of actin was evaluated comparing with localization of fibronectin, IgA and IgG by immunofluorescent microscopy on biopsied specimens with various renal diseases. In IgA nephropathy, actin was located in the expanded mesangial area and was thicker than that in minimal change disease. Hemispherical deposit was surrounded with actin. In membranous nephropathy, actin increased on the capillary loops without mesangial changes and was observed enclosing the immune deposits on GBM. Glomerular ultrastructual studies revealeded that the foot process was fused. The same findings were observed in minimal change disease but actin did not increase on the capillary loops. This suggests that thickend actin in membranous nephropathy is not caused by the foot process fusion but the other unknown mechanism, In membranoprolif erative glomerulonephritis, numerous actin was present in the expanded mesangium, whereas on the capillary loops actin did not increase. Though actin in mesangium was increased in width in patients with acute glomerulonephritis, capillary loops appeared to be normal. In lupus nephritis, the distribution patterns of actin were different according to their light microscopic findings. Actin was found surround ing the "wire-loop", but not in it. Increased mesangial actin was also found in Henoch-Schönlein purpura nephritis as same in the IgA nephropathy. Linear actin was detected in periglomerular fibrosis and no actin was detected in glomerular sclerosis. We propose the possibility that increased actin in the mesangium may lead an increase in the mesangial phagocytic function at early stage of the disease, as previously suggested by the study of increasing mesangial actin filament in phalloidin treated rats.