Postinfectious GlomerulonephritisKambham, Neeraja MDAdvances in Anatomic Pathology: September 2012 - Volume 19 - Issue 5 - p 338–347 doi: 10.1097/PAP.0b013e31826663d9 Review Articles Abstract Author Information Postinfectious glomerulonephritis (PIGN) is an immunologically mediated glomerular injury triggered by an infection. Poststreptococcal glomerulonephritis (PSGN) is a classic example of PIGN with diffuse proliferative and exudative glomerular histology, dominant C3 staining and subepithelial “humps.” Only the nephritogenic streptococcal infections cause PSGN and susceptibility to develop PSGN depends on both host and microbial factors. Over the last decade, two nephritogenic antigens, “nephritis-associated plasmin receptor” and “streptococcal pyrogenic exotoxin B” have been identified. PSGN is a self-limited disease, especially in children, but long-term follow-up studies indicate persistent low-grade renal abnormalities in a significant proportion of patients. PSGN continues to be a serious public health concern in third world countries, but the incidence of streptococcal infections has steadily declined in industrialized nations. PIGN in the western world is now primarily because of nonstreptococcal infections, often affecting older individuals with comorbidities such as diabetes mellitus or alcoholism, and is associated with poor outcomes. Although the acute PIGN has diffuse proliferative, focal segmental proliferative or mesangioproliferative patterns of glomerular injury, chronic or subacute infection-associated glomerulonephritis typically results in membranoproliferative appearance. PIGN has dominant C3 staining with frequent occurrence of subepithelial “humps” as well as subendothelial deposits. The immunoglobulin staining on immunofluorescence is typically weak, but immunoglobulin A-dominant PIGN is a recently defined entity often associated with staphylococcal infections. The wide spectrum of morphologic changes seen in PIGN poses a diagnostic challenge, especially if adequate clinical and serological data are lacking. Department of Pathology, Stanford University Medical Center, Stanford, CA The author has no funding or conflicts of interest to disclose. Reprints: Neeraja Kambham, MD, Department of Pathology, Stanford University Medical Center, Rm H2110, 300 Pasteur Drive, Stanford, CA (e-mail: email@example.com). © 2012 Lippincott Williams & Wilkins, Inc.