Ootaka T, Saito T, Soma J, Yusa A, Abe K
Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Am J Kidney Dis. 1996 Jul;28(1):40-6. doi: 10.1016/s0272-6386(96)90128-6.
Glomerular expression of intercellular adhesion molecule-1 (ICAM1) (CD54) and membrane cofactor protein (MCP; CD46) and positive infiltrating cells in leukocyte function associated antigen-1 (LFA1)alpha (CD11a) and C3bi receptors (CR3/CD11b, CR4/CD11c) were examined by the indirect immunoperoxidase method on 43 sets of repeated renal biopsy specimens from patients with immunoglobulin A nephropathy. Twenty-four-hour urine protein at the time of renal biopsy was also evaluated. Glomerular infiltration of LFA1alpha+ cells was significantly correlated with glomerular expression of ICAM1 (r = 0.494, P < 0.0001). Glomerular complement receptor type 4 (CR4)+ cells were significantly correlated with glomerular expression of MCP (r = 0.405, P < 0.0001). The glomerular expressions of ICAM1 and MCP were significantly correlated with each other (r = 0.700, P < 0.00001). The glomerular infiltrations of LFA1alpha+ and CR4+ cells were highly correlated with each other (r = 0.884, P < 0.00001), and both cell types were significantly correlated with urine protein (respectively, r = 0.426 and 0.478, P < 0.001 and 0.0001). When the change in these parameters between the time of the initial and follow-up biopsies was evaluated, there was a significant correlation between the change in glomerular expression of ICAM1 (DeltaICAM1) and MCP (DeltaMCP) as well as between the change in glomerular infiltration of LFA1alpha+ cells (DeltaLFA1alpha+) and CR4+ cells (DeltaCR4+). Both DeltaLFA1alpha+ and DeltaCR4+ were significantly correlated with the change in urine protein. These findings suggest that ICAM1/LFA1 interaction and MCP-mediated C3bi/C3biR interaction cooperate and participate in persistent glomerular infiltration of immune cells in immunoglobulin A nephropathy, and that these LFA1alpha+ and C3biR+ cells contribute to the induction of proteinuria.
采用间接免疫过氧化物酶法,对43例免疫球蛋白A肾病患者的重复肾活检标本进行检测,观察细胞间黏附分子-1(ICAM1,CD54)、膜辅因子蛋白(MCP,CD46)的肾小球表达情况,以及白细胞功能相关抗原-1(LFA1)α(CD11a)和C3bi受体(CR3/CD11b、CR4/CD11c)阳性浸润细胞情况。同时评估肾活检时的24小时尿蛋白情况。LFA1α+细胞的肾小球浸润与ICAM1的肾小球表达显著相关(r = 0.494,P < 0.0001)。肾小球4型补体受体(CR4)+细胞与MCP的肾小球表达显著相关(r = 0.405,P < 0.0001)。ICAM1和MCP的肾小球表达显著相关(r = 0.700,P < 0.00001)。LFA1α+和CR4+细胞的肾小球浸润高度相关(r = 0.884,P < 0.00001),且两种细胞类型均与尿蛋白显著相关(分别为r = 0.426和0.478,P < 0.001和0.0001)。当评估初次活检和随访活检时这些参数的变化时,ICAM1(DeltaICAM1)和MCP(DeltaMCP)的肾小球表达变化之间,以及LFA1α+细胞(DeltaLFA1α+)和CR4+细胞(DeltaCR4+)的肾小球浸润变化之间存在显著相关性。DeltaLFA1α+和DeltaCR4+均与尿蛋白变化显著相关。这些发现提示,ICAM1/LFA1相互作用和MCP介导的C3bi/C3biR相互作用协同参与免疫球蛋白A肾病中免疫细胞的持续性肾小球浸润,且这些LFA1α+和C3biR+细胞有助于蛋白尿的产生。