Pathologic Findings Light Microscopy

By light microscopy, the acute glomerular lesion is characterized by segmental to global fibrinoid necrosis with crescent formation in over 90% of

Table 9.1. Frequency of immunopathologic categories of crescentic glomerulonephritis in over 3000 consecutive native kidney biopsies evaluated by immunofluorescence microscopy in the University of North Carolina Nephropathology Laboratory

Any crescents

>50% crescents

Arteritis in biopsy

(n = 487)

(n = 195)

(n = 37)

Immunohistology

Pauciimmune

47% (227/487)

61% (118/195)a

84% (31/37)

(<2+ Ig)

Immune complex

49% (238/487)

29% (56/195)

14% (5/37)c

(>2+ Ig)

Anti-GBM

5% (25/487)b

11% (21/195)

3% (1/37)d

a 70 of 77 patients tested for ANCA were positive (91%) (44 P-ANCA and 26 C-ANCA). b 3 of 19 patients tested for ANCA were positive (16%) (2 P-ANCA and 1 C-ANCA). c 4 patients had lupus and 1 post-streptococcal glomerulonephritis. d This patient also had a P-ANCA (MPO-ANCA). From Jennette and Falk (3).

a 70 of 77 patients tested for ANCA were positive (91%) (44 P-ANCA and 26 C-ANCA). b 3 of 19 patients tested for ANCA were positive (16%) (2 P-ANCA and 1 C-ANCA). c 4 patients had lupus and 1 post-streptococcal glomerulonephritis. d This patient also had a P-ANCA (MPO-ANCA). From Jennette and Falk (3).

patients (1). Periodic acid-schiff (PAS) and silver stains demonstrate breaks in the GBM in areas of necrosis (Fig. 9.1). Glomerular segments that do not have necrosis often are remarkably normal or have a slight increase in neutrophils. Marked neutrophil infiltration is observed in association with the necrosis in occasional specimens. Features of aggressive immune complex glomerulonephritis are notably absent, such as marked capillary wall thickening and endocapillary hypercellularity. Often there are breaks

Figure 9.1. Glomerulus from a patient with anti-glomerular basement membrane (GBM) disease showing a very large cellular crescent and extensive destruction of approximately 80% of the tuft. A few silver-positive intact profiles of GBM are present at the hilum (Jones silver stain).
Imajenes Musica
Figure 9.2. Glomerulus from a patient with anti-GBM disease showing linear staining of the GBM by direct immunofluorescence microscopy using an antibody specific for immunoglobulin G (IgG).

in Bowman's capsule, occasionally with associated reactive multinucleated giant cells (5).

With time, foci of glomerular necrosis evolve into glomerular sclerosis, and cellular crescents become fibrous crescents. Acute tubulointerstitial inflammation that is centered on necrotic glomeruli evolves to more regional or generalized interstitial fibrosis with chronic inflammation and tubular atrophy.

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