Acute post streptococcal glomerulonephritis
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  • 1. • Acute ProliferativeGlomerulonephritis Lecture 45 Acute Poststreptococcal Glomerulonephritis
  • 2. Acute Poststreptococcal Glomerulonephritis • Acute glomerulonephritis is a disease characterized by the sudden appearance of edema, hematuria, proteinuria, and hypertension.
  • 3. APSGN • It is a representative disease of acute nephritic syndrome in which inflammation of the glomerulus is manifested by proliferation of cellular elements secondary to an immunologic mechanism.
  • 4. Acute Proliferative (Poststreptococcal, Postinfectious) Glomerulonephritis Characterized histologically by • diffuse proliferation of glomerular cells, associated with influx of leukocytes. • Occurs predominantly in males 97 percent occur in developing countries
  • 5. Acute Poststreptococcal Glomerulonephritis • These lesions are typically caused by immune complexes. • The inciting antigen may be exogenous (Postinfectious glomerulonephritis) or •endogenous (SLE).
  • 6. Acute Proliferative Glomerulonephritis • The most common underlying infections are streptococcal, but the disorder also has been associated with other infections.
  • 7. APSGN • It usually appears 1 to 4 weeks after a streptococcal infection of the pharynx or skin. • It occurs most frequently in children 6 to 10 years of age, but adults of any age can also be affected.
  • 8. Etiology and Pathogenesis. Only certain strains of group A β-hemolytic streptococci are nephritogenic, more than 90% of cases being traced to types 12, 4, and 1, which can be identified by typing of M protein of the cell wall. The M and T proteins in the bacterial wall have been used for characterizing streptococci. Nephritogenicity is mainly restricted to certain M protein serotypes (ie, 1, 2, 4, 12, 18, 25, 49, 55, 57, and 60) that have shown nephritogenic potential.
  • 9. Etiology & Pathogenesis of Ac Prolif. G • Poststreptococcal glomerulonephritis is an immunologically mediated disease. • Elevated titers of antibodies against one or more streptococcal antigens are present in a great majority of patients.
  • 10. Etiology & Pathogenesis of Ac Prolif. G • Serum complement levels are low, • There are granular immune deposits in the glomeruli, supporting an immune complex–mediated mechanism. The resulting glomerular immune complex disease triggers complement activation and inflammation.
  • 11. Pathogenesis • The 2 most widely proposed theories include (1) glomerular trapping of circulating immune complexes and • (2) in situ immune antigen-antibody complex formation resulting from antibodies reacting with either streptococcal components deposited in the glomerulus or with components of the glomerulus itself, which has been termed “molecular mimicry.”
  • 12. Etiology & Pathogenesis • Several cationic antigens, including a nephritis-associated streptococcal plasmin receptor (NAPlr), unique to nephritogenic strains of streptococci, can be found in affected glomeruli.
  • 13. Etiology & PathogEnEsis • Streptococcal pyogenic exotoxin B (SpeB) and its zymogen precursor (zSpeB), are the principal antigenic determinants in most cases of poststreptococcal glomerulonephritis.
  • 14. Morphology Light microscopy  It shows a diffuse proliferative glomerulonephritis with prominent endocapillary proliferation and numerous neutrophils.  Trichrome stain may show small subepithelial hump-shaped deposits. Crescent formation is uncommon and is associated with a poor prognosis.
  • 15. Light microscopic findings Early stage → glomerular hypercellularity Later stage → Proliferation of intrinsic endothelial & mesangial cells
  • 16. Immunofluorescence microscopy • Shows a characteristic pattern of deposits of immunoglobulin (IgG) and C3 distributed in a diffuse granular pattern within the mesangium, and glomerular capillary walls. • Other immune reactants (eg, IgM, IgA, fibrin, and other complement components) may also be detected.
  • 17. Electron microscopy The dome-shaped subepithelial electron-dense deposits that are referred to as humps. Subendothelial immune deposits and subsequent complement activation are responsible for the local influx of inflammatory cells, leading to a proliferative glomerulonephritis, an active urine sediment, and a variable decline in glomerular filtration rate. Subepithelial "humps" are responsible for epithelial cell damage and proteinuria, similar to that seen in membranous nephropathy
  • 18. Clinical Features Of APG History: In the classic case, a young child abruptly develops malaise, fever, nausea, oliguria, and hematuria 1 to 2 weeks after recovery from a sore throat.
  • 19. Clinical features of Acute Proliferative Glomerulonephritis The patients have red cell casts in the urine, mild proteinuria (usually less than 1 gm/day), periorbital edema, and mild to moderate hypertension.
  • 20. Clinical features of Acute Proliferative Glomerulonephritis In adults the onset is more likely to be atypical, such as the sudden appearance of hypertension or edema, frequently with elevation of BUN.
  • 21. Clinical features of Acute Proliferative Glomerulonephritis • During epidemics caused by nephritogenic streptococcal infections, glomerulonephritis may be asymptomatic, discovered only on screening for microscopic hematuria.
  • 22. Laboratory Findings • Elevations of antistreptococcal antibody titers and • a decline in the serum concentration of C3 and other components of the complement cascade.
  • 23. Prognosis • More than 95% of affected children eventually recover totally with conservative therapy aimed at maintaining sodium and water balance. • A small minority of children (perhaps fewer than 1%) do not improve, become severely oliguric, and develop a rapidly progressive form of glomerulonephritis.
  • 24. Nonstreptococcal Acute Glomerulonephritis (Postinfectious Glomerulonephritis) Glomerulonephritis occurs sporadically in association with other infections, including bacterial viral and parasitic. Granular immunofluorescent deposits and subepithelial humps are present.