title: Glomerular expression of plasmalemmal vesicle-associated protein-1 in patients with transplant glomerulopathy.
abstract: Transplant glomerulopathy (TG) is a prominent feature of chronic rejection that is characterized by double contours of the glomerular capillaries (GC). In this report, we demonstrate that one of the histopathological features of TG is a phenotypic change of glomerular endothelial cells which is illustrated by increased caveolae formation. To verify the endothelial changes in this disease, we examined the expression of plasmalemmal vesicle-associated protein-1 (PV-1), a glycoprotein associated with plasmalemmal vesicles (caveolae), in the glomeruli of TG patients using pathologische anatomie Leiden-endothelium (PAL-E) antibody. Twenty-six cases of chronic allograft nephropathy (CAN) with TG were examined, compared with 16 cases of CAN without TG, type I MPGN (4 cases), and transplant glomerulitis (8 cases). Overall, 24 of 26 (92.3%), 4 of 16 (25%), 0 of 4, 0 of 8 cases were PAL-E-positive for GC, respectively. Further, the extent of glomerular PAL-E expression was positively correlated with both the grade of TG (rs= 0.72, p = 0.0003) and proteinuria (g/day) (rs= 0.51, p = 0.02). A correlation was not observed between glomerular PAL-E positivity and peritubular capillary C4d deposits (Yetes chi = 0.23, p = 0.89). In summary, the present study demonstrates expression of PV-1 in the GC of TG which is correlated with the grade of TG and proteinuria.
authors.affiliation: Department of Internal Medicine, Division of Kidney and Hypertension, The Jikei University School of Medicine. izumi26@jikei.ac.jp
authors.forename: I
authors.initials: I
authors.lastname: Yamamoto
authors.forename: S
authors.initials: S
authors.lastname: Horita
authors.forename: T
authors.initials: T
authors.lastname: Takahashi
authors.forename: K
authors.initials: K
authors.lastname: Tanabe
authors.forename: S
authors.initials: S
authors.lastname: Fuchinoue
authors.forename: S
authors.initials: S
authors.lastname: Teraoka
authors.forename: M
authors.initials: M
authors.lastname: Hattori
authors.forename: Y
authors.initials: Y
authors.lastname: Yamaguchi
mesh_terms: D000293:Adolescent; D000328:Adult; D000911:Antibodies, Monoclonal / Q000276:immunology; D001706:Biopsy; D002352:Carrier Proteins / Q000096:biosynthesis* / Q000276:immunology; D021941:Caveolae / Q000378:metabolism; D002908:Chronic Disease; D015935:Complement C4b / Q000276:immunology / Q000378:metabolism; D018450:Disease Progression; D042783:Endothelial Cells / Q000648:ultrastructure; D004730:Endothelium, Vascular / Q000648:ultrastructure; D005260:Female; D005500:Follow-Up Studies; D006084:Graft Rejection / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D007678:Kidney Glomerulus / Q000378:metabolism* / Q000648:ultrastructure; D016030:Kidney Transplantation; D008297:Male; D008565:Membrane Proteins / Q000096:biosynthesis* / Q000276:immunology; D008854:Microscopy, Electron; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000150:complications* / Q000473:pathology; D010446:Peptide Fragments / Q000276:immunology / Q000378:metabolism; D011379:Prognosis; D012189:Retrospective Studies; D012720:Severity of Illness Index
chemical_list: D000911:Antibodies, Monoclonal; D002352:Carrier Proteins; D008565:Membrane Proteins; C486771:PLVAP protein, human; D010446:Peptide Fragments; D015935:Complement C4b; C032261:complement C4d