Iwama H, Horikoshi S, Shirato I, Tomino Y
Department of Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Am J Kidney Dis. 1998 Nov;32(5):785-93. doi: 10.1016/s0272-6386(98)70134-9.
To determine the relationship between the detection of Epstein-Barr virus (EBV)-specific DNA and glomerular injury, 33 renal needle-biopsy specimens that had been formalin-fixed and paraffin-embedded were analyzed using polymerase chain reaction (PCR) with subsequent nonradioactive Southern blot technique. Light microscopic examination and immunofluorescence were also performed. In 30 of 33 renal biopsy specimens, the beta globin gene could be successfully amplified as integrity controls. These 30 patients consisted of 12 patients with immunoglobulin A nephropathy (IgAN), 10 patients with minor glomerular abnormalities, 6 patients with membranous nephropathy, and 2 patients with focal/segmental lesions. EBV was detected in 7 of 12 patients with IgAN (58%), 3 of 6 patients with membranous nephropathy (50%), 0 of 10 patients with minor glomerular abnormalities (0%), and 2 of 2 patients with focal/segmental lesions. EBV detection was not disease specific. The EBV detection ratio of the group with glomerular mesangial lesions (64%; 9 of 14 patients) was significantly greater than those without (19%; 3 of 16 patients; P < 0.012, chi-square test). The EBV detection ratio of the group with glomerular lesions (60%; 12 of 20 patients) was significantly greater than those without (0%; 0 of 10 patients; P < 0.0016, Fisher's exact test), and the EBV detection ratio of the group with fibrinogen deposits observed in immunofluorescence (73%; 11 of 15 patients) was significantly greater than those without (7%; 1 of 15 patients; P < 0.0002, chi-square test). The EBV detection ratio of the group with immunoglobulin deposits (57%; 12 of 21 patients) was also significantly greater than those without (0%; 0 of 9 patients; P < 0.0040, Fisher's exact test). These data suggest that EBV can damage the glomerular mesangium beyond disease units and be mediated by immunoglobulin in patients with various chronic glomerulonephritides.
为确定爱泼斯坦-巴尔病毒（EBV）特异性DNA检测与肾小球损伤之间的关系，我们使用聚合酶链反应（PCR）及随后的非放射性Southern印迹技术，对33份经福尔马林固定和石蜡包埋的肾穿刺活检标本进行了分析。同时还进行了光镜检查和免疫荧光检查。在33份肾活检标本中的30份中，β珠蛋白基因可作为完整性对照成功扩增。这30例患者包括12例免疫球蛋白A肾病（IgAN）患者、10例轻度肾小球异常患者、6例膜性肾病患者和2例局灶性/节段性病变患者。在12例IgAN患者中有7例（58%）检测到EBV，6例膜性肾病患者中有3例（50%），10例轻度肾小球异常患者中0例（0%），2例局灶性/节段性病变患者中有2例。EBV检测并非疾病特异性的。肾小球系膜病变组的EBV检测率（64%；14例患者中的9例）显著高于无系膜病变组（19%；16例患者中的3例；卡方检验，P<0.012）。有肾小球病变组的EBV检测率（60%；20例患者中的12例）显著高于无病变组（0%；10例患者中的0例；Fisher精确检验，P<0.0016），免疫荧光观察到有纤维蛋白原沉积组的EBV检测率（73%；15例患者中的11例）显著高于无沉积组（7%；15例患者中的1例；卡方检验，P<0.0002）。有免疫球蛋白沉积组的EBV检测率（57%；21例患者中的12例）也显著高于无沉积组（0%；9例患者中的0例；Fisher精确检验，P<0.0040）。这些数据表明，在各种慢性肾小球肾炎患者中，EBV可损害肾小球系膜，且这种损害超出疾病单元范围，并由免疫球蛋白介导。
