The Expression And Significance Of α-SMA In Human Chronic Kidney Disease

Objective:To explore and disscuss the express division ofα-smooth muscle actin in the chronic nephropathy patient and its connection with clinical situation.Methods:checking the expressive level ofα-SMA in actinus renis and nephric tubule of 40 chronic nephropathy patients through S-P,then making statistics analysis with the clinical information and pathology of nephropathy.Results: 1.α-SMA in renal tissue in the control group only express in the vascular smooth muscle cells,with of glomerular and tubular,almost no expression;in patients with chronic kidney disease,kidney tissue lesions were positive forα-SMA,and normal control group compared to patients with chronic kidney disease in renal glomerular mesangial area,Bowman capsule and renal interstitialα- SMA were positive in the expression level compared with normal control group was statistically significantly different(P＜0.01).2.Proliferative glomerulonephritis glomerulus and renal tubules were positive forα-SMA expression compared with control group,the difference was significant(P＜0.01).Light,moderate and severe mesangial proliferative group of mesangial cell proliferation with the severity of,α-SMA in glomerular and tubular expression increased,between severe mesangial proliferation and moderate mesangial proliferative group,between moderate mesangial proliferative group compared with mild mesangial proliferative glomerular and tubular expression were significantly different(P＜0.05),Compared with severe mesangial proliferative group and the mild mesangial proliferative,glomerular and tubular group was statistically significant significance(P＜0.01).3.Membranous nephropathy(MN) of glomeruli and tubules were positive forα-SMA expression compared with control group,the difference was significant(P＜0.01).Between MN group StageⅢand StageⅡ,Between MN group StageⅡand StageⅠ,MN group of glomerular and tubular expression ofα-SMA was significant(P＜0.05),ⅢandⅠgroup of MN group of glomerular and tubular expression ofα-SMA are statistically significant(P＜0.01).4.sclerosing glomerulonephritis glomerulus and tubular expression ofα-SMA positive,compared with control group,the difference was significant(P＜0.01).5.The glomerular pathology between the two groups,andα-SMA expression in renal tubular area had no significant difference(P＞0.05).6.α-SMA and the clinical parameters of:α-SMA and serum creatinine,blood urea nitrogen,24-hour urinary protein were significantly positive,correlationcoefficients were(r=0.768,0.620),(r=0.701,0.618),(r=0.674,0.693), and lipids,albumin not related.Conclusion:1.α-smooth muscle actin(α-SMA) in normal kidney almost no expression,only in the renal tissue of vascular smooth muscle cells to express,and in the kidney disease group ball and in the tubular expression ofα-SMA were positive.2.Proliferative glomerulonephritis group, mesangial cell proliferation with the severity of,α-SMA in glomerular and tubular expression increased,suggesting thatα-SMA in mesangial cells can be damaged as the activation and phenotype signs reflect the state of mesangial cell function and proliferation.3.Membranous nephropathy(MN) groups,each of MN glomerular and tubular expression ofα-SMA were increased and were positively correlated with the degree of glomerular damage(r =0.615,P＜0.05),and tubulo degree of injury is related to quality(r =0.907,P＜0.05),suggest the inherent renal cell -myofibroblast transdifferentiation in MN advances of great significance.4.Sclerosing glomerulonephritis glomerulus and tubular expression ofα-SMA positive,compared with control group,the difference was significant(P＜0.01),kidney prompted the expression ofα-SMA increased participation in glomerular hardening of the occurrence and development.5.α-SMA and serum creatinine,blood urea nitrogen, 24-hour urinary protein were significantly positively correlated,suggesting thatα-SMA is caused by impaired renal function,one of the main factors,it will become a new renal fibrosis the target.