The glomerulus is enlarged and hypercellular, showing an influx of leukocytes and monocytes. There is also a proliferation of mesangial and endothelial cells and in advanced cases, crescent formation may be present. The capillary lumens may be obliterated as seen here, as a result of endothelial proliferation and infiltration of inflammatory cells (Kumar, Cheng). Tubulointerstitial edema frequently accompanies glomerular injury.
Immunofluorescence microscopy on this case demonstrates very coarse lumpy bumpy staining for IgG along the GBM. Note that IgM and C3 are also present in the immune complexes.
Large subepithelial humps can be appreciated on EM (arrows on humps).
Check out this super large subepithelial hump and be impressed.
Postinfectious glomerulonephritis (PIGN) can be caused by a number of infectious agents. When it is caused by beta-hemolytic Streptococcus, it is referred to as poststreptococcal glomerulonephritis (PSGN). PSGN is more common in children, whereas PIGN secondary to systemic infections (e.g. endocarditis, abscesses in other viscera) are more common adults (Kumar).
Circulating immune complexes containing antibodies to streptococcal antigens and complement are deposited in the glomeruli. Deposits of IgG, IgM and C3 in the basement membrane and mesangium is seen on IF, creating a granular pattern. On EM, subepithelial deposits "humps" are typically seen, although smaller deposits in the subendothelium and mesangium may also be present.
Presents with nephritic syndrome (hematuria, edema, hypertension, oliguria). PSGN usually affects children age 6-10 years. There is usually a history of a strep throat or a skin infection (impetigo) 2-3 weeks prior to the onset of renal symptoms. Titers of anti-streptococcal antibodies (ASO) are elevated, serum complement levels are low indicating activation of the complement system.
In children, 95% of cases are self-limited disease which resolves within several weeks. In adults, however, only 60% resolve quickly -- some develop chronic glomerulonephritis and even rapidly progressive glomerulonephritis.
Cheng L, Bostwick DG, eds. Essentials of Anatomic Pathology. 2nd Ed. Totowa, NJ: Humana Press; 2006: 1123-4.
Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease. 7th Ed. Philadelphia, PA: Elsevier; 2005: 973-6.
Zhou M, Magi-Galluzzi, C. Genitourinary Pathology: Foundations in Diagnostic Pathology. Philadelphia, PA: Elvesier; 2006: 368-70.