Kidney nontumor
Primary glomerular diseases
Post-infectious glomerulonephritis

Author: Nikhil Sangle, M.D. (see Authors page)

Revised: 30 October 2017, last major update March 2014

Copyright: (c) 2003-2017, PathologyOutlines.com, Inc.

PubMed Search: Post-infectious glomerulonephritis
Cite this page: Sangle, N. Post-infectious glomerulonephritis. PathologyOutlines.com website. http://pathologyoutlines.com/topic/kidneypoststrep.html. Accessed November 21st, 2017.
Definition / general
  • Also called post streptococcal or acute glomerulonephritis; a type of diffuse endocapillary proliferative glomerulonephritis
Pathophysiology
  • Deposition of immune complexes from antibodies against organisms elicits acute inflammatory response and nephritic syndrome
  • Associated with nephritogenic strains of Streptococcus pyogenes (beta hemolytic Strep group A)
  • Similar histologic findings also associated with endemic malaria, toxoplasmosis, hepatitis B/C, HIV, varicella, spirochetes, staphylococci (Clin J Am Soc Nephrol 2006;1:1179), meningococci and other bacteria
  • Similar process occurs in response to endogenous antigen in SLE
Diagrams / tables

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Diagram

Clinical features
  • Post-streptococcal disease is decreasing in US (eMedicine - Poststreptococcal Glomerulonephritis)
  • 95% recover with conservative therapy; 1% develop rapidly progressive glomerulonephritis, 1 - 2% develop chronic glomerulonephritis
  • Poor prognosis more likely if massive proteinuria and abnormal GFR; 2 - 5% die from pulmonary edema, hypertensive encephalopathy or crescentic glomerulonephritis; children with obesity may have greater renal injuries (Clin Nephrol 2009;71:632)
  • Children age 6 - 10: nephritic presentation with abrupt onset of hematuria, oliguria, fever, malaise and nausea 1 - 4 weeks after strep infection of pharynx or skin (impetigo); RBC casts, proteinuria, periorbital edema and hypertension
  • Adults: may have atypical presentation with sudden hypertension, edema and elevated BUN; 60% recover, others develop rapidly progressive glomerulonephritis (Arab J Nephrol Transplant 2012;5:93, J Med Assoc Thai 2006;89 Suppl 2:S157)
  • Laboratory (children and adults): high antistreptococcal antibody titers, low C3 (due to consumption)

    Subclinical:
  • Typical immune complex deposition of clinical disease, but with minimal symptoms or urinary abnormalities
  • Important to recognize, since present in 10% of renal biopsies (Hum Pathol 2003;34:3)
Case reports
Microscopic (histologic) description
  • Glomeruli are globally and diffusely enlarged and hypercellular due to neutrophils and macrophages and proliferation of mesangial and endothelial cells (also called ‘exudative’ glomerulonephritis)
  • Swelling of endothelial cells and presence of inflammatory cells obstructs capillary lumina
  • Returns to normal within months
  • Slight mononuclear leucocytic infiltrate and edema in the interstitium
  • Tubules contain red blood cells
Microscopic (histologic) images

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Various images

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Markedly hypercellular glomeruli due to neutrophils

Immunofluorescence
  • Lumpy bumpy (granular) deposition of IgG, IgM and C3 in peripheral glomerular loops
  • Also properdin; no C1q or C4
Immunofluorescence images

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Lumpy bumpy (granular) or starry scar immunofluoresence

Electron microscopy description
  • Subepithelial ‘humps’ (finely granular, dome-shaped, electron dense, representing immune complex deposits), no spikes (compare to membranous glomerulonephritis)
  • Obliteration of epithelial cell foot processes
  • Subepithelial, intramembranous, subendothelial and mesangial deposits in the acute phase