| Glomerular disease |
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| Glomerular disease with systemic lupus erythematosus (SLE) is common, and lupus nephritis can have many morphologic manifestations as seen on renal biopsy. In general, the more immune complex deposition and the more cellular proliferation, the worse the disease. In this case, there is extensive immune complex deposition in the thickened glomerular capillary loops, giving a so-called wire loop appearance |
| membranoproliferative glomerulonephritis |
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| This is membranoproliferative glomerulonephritis (MPGN). Those cases that are idiopathic are divided into types I and II by pathologic findings. As seen here, the glomerulus has increased overall cellularity, mainly increased mesangial cellularity |
| immunofluorescence micrograph of a glomerulus |
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| This immunofluorescence micrograph of a glomerulus demonstrates positivity with antibody to fibrinogen. With a rapidly progressive GN, the glomerular damage is so severe that fibrinogen leaks into Bowman's space, leading to proliferation of the epithelial cells and formation of the bright crescent shown here |
| crescents |
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| Seen here within the glomeruli are crescents composed of proliferating epithelial cells. Crescentic glomerulonephritis is known as rapidly progressive glomerulonephritis (RPGN) because this disease is very progressive. There are several causes, and in this case is due to SLE. Note in the lower left glomerulus that the capillary loops are markedly thickened (the so-called "wire loop" lesion of lupus nephritis |
| spikes" seen with membranous glomerulonephritis |
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| A silver stain of the glomerulus highlights the proteinaceous basement membranes in black. There are characteristic "spikes" seen with membranous glomerulonephritis seen here in which the black basement membrane material appears as projections around the capillary loops |
| 334) Post-infectious glomerulonephritis |
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| Post-infectious glomerulonephritis is immunologically mediated, and the immune deposits are distributed in the capillary loops in a granular, bumpy pattern because of the focal nature of the immune complex deposition process |
| membranoproliferative glomerulonephritis, type II |
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| The bright deposits scattered along capillary walls and in the mesangium by immunofluorescence microscopy with antibody to complement component C3 are typical for membranoproliferative glomerulonephritis, type II. MPGN type II, known as dense deposit disease, produces a nephritic syndrome. Most patients have detectable circulating C3 nephritic factor, an IgG autoantibody |
| IgA nephropathy |
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| This immunofluorescence pattern demonstrates positivity with antibody to IgA. Note that the pattern is that of mesangial deposition in the glomerulus. This is IgA nephropathy |
| glomerulus |
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| This immunofluorescence micrograph of a glomerulus demonstrates positivity with antibody to fibrinogen. With a rapidly progressive GN, the glomerular damage is so severe that fibrinogen leaks into Bowman's space, leading to proliferation of the epithelial cells and formation of the bright crescent shown here |
| membranous glomerulonephritis |
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| By electron microscopy in membranous glomerulonephritis, the darker electron dense immune deposits are seen scattered within the thickened basement membrane. The "spikes" seen with the silver stain represent the intervening matrix of basement membrane between the deposits |
| membranous glomerulonephritis |
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| Here is the light microscopic appearance of membranous glomerulonephritis in which the capillary loops are thickened and prominent, but the cellularity is not increased. Membranous GN is the most common cause for nephrotic syndrome in adults. Some cases of membranous GN can be linked to a chronic infectious disease such as hepatitis B, a carcinoma, or SLE, but many cases are idiopathic |
| hypercellularity of post-infectious glomerulonephritis |
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| The hypercellularity of post-infectious glomerulonephritis is due to increased numbers of epithelial, endothelial, and mesangial cells as well as neutrophils in and around the glomerular capillary loops. This disease may follow several weeks after infection with certain strains of group A beta hemolytic streptococci. Patients who have had a strep infection typically have an elevated anti-streptolysin O (ASO) titer |
| membranous glomerulonephritis |
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| Here is the light microscopic appearance of membranous glomerulonephritis in which the capillary loops are thickened and prominent, but the cellularity is not increased. Membranous GN is the most common cause for nephrotic syndrome in adults. Some cases of membranous GN can be |
| membranoproliferative glomerulonephritis type II |
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| The electron micrograph above demonstrates dense deposits in the basement membrane typical for MPGN type II. These dark electron dense deposits within the basement membrane often coalesce to form a ribbon-like mass of deposits, as seen in the electron micrograph below |
| Berger disease |
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| This is IgA nephropathy (Berger disease). The IgA is deposited mainly within the mesangium, which then increases mesangial cellularity as shown at the arrow. Patients with IgA nephropathy usually present with hematuria |
| glomerulus with epithelial crescents |
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| 341) Here is another glomerulus with epithelial crescents squashing the glomerular tufts from all sides. RPGN may be idiopathic or may result from SLE, post-infectious GN (as in some cases of post-infectious GN), from various types of vasculitis, and from Goodpasture syndrome |
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