Epstein-Barr virus detection in kidney biopsy specimens correlates with glomerular mesangial injury.
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.
Iwama
H
H
Department of Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Horikoshi
S
S
Shirato
I
I
Tomino
Y
Y
D001707:Biopsy, Needle; D015139:Blotting, Southern; D016009:Chi-Square Distribution; D003176:Complement C3 / Q000032:analysis; D004279:DNA, Viral / Q000032:analysis / Q000235:genetics; D020031:Epstein-Barr Virus Infections / Q000175:diagnosis* / Q000473:pathology; D005340:Fibrinogen / Q000032:analysis; D005455:Fluorescent Antibody Technique; D005914:Globins / Q000235:genetics; D005921:Glomerulonephritis / Q000473:pathology / Q000821:virology*; D005922:Glomerulonephritis, IGA / Q000473:pathology / Q000821:virology; D015432:Glomerulonephritis, Membranoproliferative / Q000473:pathology / Q000821:virology; D015433:Glomerulonephritis, Membranous / Q000473:pathology / Q000821:virology; D005923:Glomerulosclerosis, Focal Segmental / Q000473:pathology / Q000821:virology; D004854:Herpesvirus 4, Human / Q000235:genetics / Q000302:isolation & purification*; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis; D007074:Immunoglobulin G / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D007678:Kidney Glomerulus / Q000473:pathology / Q000821:virology*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction
D003176:Complement C3; D004279:DNA, Viral; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D005340:Fibrinogen; D005914:Globins