ATLAS OF RENAL PATHOLOGY
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Membranoproliferative Glomerulonephritis
Pathology Editor: Agnes Fogo, MD
Medical Photographer: Brent Weedman
With Assistance From the National Kidney Foundation's cyberNephrologyTM Team: Kim Solez, MD, Director; Joseph DeAlmeida, Computer Engineer; and Brenda Kalynchuk, Administrative Assistant
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Fig 1. Diffuse lobular simplification of glomeruli in membranoproliferative glomerulonephritis type 1, caused by
extensive endocapillary proliferation (Jones' silver stain; original magnification, x100). |
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Fig 2. Extensive double contours of the glomerular basement membranes, stained by silver, in
membranoproliferative glomerulonephritis type 1, caused by mesangial interposition and new basement membrane
formation in response to subendothelial immune complex deposits. The deposits are PAS positive and
globular-to-sausage shaped (Jones' silver stain; original magnification, x400). |
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Fig 3. Segmental, coarsely granular-to-globular or elongated capillary wall IgG deposits in membranoproliferative
glomerulonephritis type 1 (immunofluorescence with anti-IgG; original magnification, x200). |
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Fig 4. Segmental, irregular, coarsely granular, or elongated deposits along the capillary wall and occasional
mesangial IgG deposits are typical of membranoproliferative glomerulonephritis type 1 (immunofluorescence with
anti-IgG; original magnification, x200). |
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Fig 5. The subendothelial location of these segmental, irregular IgG capillary wall deposits can be deduced by their
smooth outer contour, caused by molding against the glomerular basement membrane. These deposits are typical
of membranoproliferative glomerulonephritis type 1 (immunofluorescence with anti-IgG; original magnification,
x200). |
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Fig 6A. In secondary forms of immune complex-mediated membranoproliferative glomerulonephritis (such as those
caused by chronic infections), the deposits and proliferation are commonly more focal and segmental than in
idiopathic membranoproliferative glomerulonephritis type 1 (see Figs 1 and 3). In Fig 6A, sharply segmental IgG and C3 capillary wall deposits are present (immunofluorescence with anti-IgG;
original magnification, x100). |
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Fig 6B. In secondary forms of immune complex-mediated membranoproliferative glomerulonephritis (such as those
caused by chronic infections), the deposits and proliferation are commonly more focal and segmental than in
idiopathic membranoproliferative glomerulonephritis type 1 (see Figs 1 and 3). In Fig 6B, large subendothelial deposits molding under the glomerular basement membrane and occasional
mesangial deposits are present (immunofluorescence with anti-C3; original magnification, x400). |
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Fig 7. Membranoproliferative glomerulonephritis type 1. The marked endocapillary proliferation (proliferating
endothelial and mesangial cells) appears to occlude the capillary lumen. Numerous large subendothelial and
occasional mesangial-dense immune complex-type deposits (bottom middle) are present (transmission electron
microscopy; original magnification, x4,700). |
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Fig 10A. Membranoproliferative glomerulonephritis type 1. In Fig 10A, a small subendothelial deposit lies between the glomerular basement membrane and an interposed
mesangial cell, extending from the mesangial area seen on the right. Between the interposed mesangial cell, and the
endothelium, new basement membrane material is present (transmission electron microscopy; original magnification,
x6,300). |
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Fig 10B. Membranoproliferative glomerulonephritis type 1.
In Fig 10B, mesangial interposition is illustrated at higher magnification, without evident deposits. These changes
result in a "tram-track," double contour of the basement membrane by light microscopy (see Fig 2) (transmission
electron microscopy; original magnification, x54,000). |
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Fig 11. Although subepithelial hump-shaped deposits are characteristic of acute postinfectious glomerulonephritis,
occasionally such deposits may be present in membranoproliferative glomerulonephritis type 1, as shown in this
case, in addition to the typical subendothelial deposits (original magnification, x16,000). |
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From the Department of Pathology, Vanderbilt University Medical Center,
Nashville, TN.
Received December 12, 1997; accepted as is December 12, 1997.
Address author queries to Agnes Fogo, MD, Department of Pathology,
Vanderbilt University Medical Center, MCN C-3310, Nashville, TN 37232.
E-mail:Agnes.Fogo@vanderbilt.edu
Am J Kidney Dis 31(1):E1, 1998 (available www.ajkd.org)
Copyright © 1998 by the National Kidney Foundation, Inc.
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