This document discusses acute glomerulonephritis, specifically acute post-streptococcal glomerulonephritis (APSGN). It begins by introducing acute glomerulonephritis and dividing it into post-streptococcal and non-streptococcal types. It then focuses on APSGN, describing how it typically affects children after a streptococcal throat or skin infection. The pathogenesis involves an immune response against streptococcal antigens. Clinically, APSGN presents as acute nephritic syndrome with hematuria, proteinuria, hypertension, and edema. Microscopically, there is proliferation of glomerular cells and neutrophil infiltration.

1. The KIDNEY
Acute
Glomerulonephritis
DR. ROOPAM JAIN
PROFESSOR & HEAD, PATHOLOGY

2. I. PRIMARY GLOMERULONEPHRITIS
• Acute Glomerulonephritis
• Synonyms:
• Acute Diffuse Proliferative GN,
• Diffuse Endocapillary GN

3. Acute Glomerulonephritis
• Acute GN is known to follow acute infection and characteristically
presents as acute nephritic syndrome.
• Based on etiologic agent, acute GN is subdivided into 2 main groups:
• acute post-streptococcal GN & (more common)
• acute non-streptococcal GN

4. ACUTE POST-STREPTOCOCCAL GN (APSGN)
• common form of GN in developing countries,
• mostly affecting children between 2 to 14 years of age but 10% cases
are seen in adults above 40 years of age.
• The onset of disease is generally sudden after 1-2 weeks of
streptococcal infection, most frequently of the throat (e.g. streptococcal
pharyngitis) and sometimes of the skin (e.g. streptococcal impetigo).

5. ACUTE POST-STREPTOCOCCAL GN (APSGN)
ETIOPATHOGENESIS
• The relationship between streptococcal infection and this form of GN is now well establish
• The evidences cited in support are as under:
• i) There is epidemiological evidence of preceding streptococcal sore throat or skin infection
about 1-2 weeks prior to the attack.
• ii) The latent period between streptococcal infection and onset of clinical manifestations of
the disease is compatible with the period required for building up of anti bodies.
• iii) Streptococcal infection may be identified by culture or may be inferred from elevated
titres of antibodies against streptococcal antigens.
• a) anti-streptolysin O (ASO);
• b) anti-deoxyribonuclease B (anti-DNAse B);
• c) anti-streptokinase (ASKase);
• d) anti-nicotinyl adenine dinucleotidase (anti-NADase); and
• e) anti-hyaluronidase (AHase).
• iv) hypocomplementaemia indicating involvement of complement in the glomerular deposits.
• v) identify antigenic component of streptococci which is cytoplasmic antigen, endostreptosin.

6. Acute post-streptococcal GN
Light microscopic appearance. There is increased cellularity due to proliferation of
mesangial cells, endothelial cells and some epithelial cells and infi ltration of the tuft by
neutrophils and monocytes.

7. APSGN - MORPHOLOGIC FEATURES - GROSS
• Grossly, the kidneys are
symmetrically enlarged,
weighing one and a half to
twice the normal weight. Th
e cortical as well as sectio
ned surface show petechial
haemorrhages giving the
characteristic appearance of
fl ea-bitten kidney (Fig
Flea-bitten kidney
The kidney is enlarged in size and
weight.
The cortex shows tiny petechial
haemorrhages visible through

8. Acute
glomerulonephritis
Diagrammatic representation of ultrastructure of a portion of glomerular
lobule showing
characteristic electron-dense irregular deposits or ‘humps’
on the epithelial side of the GBM

9. ACUTE POST-STREPTOCOCCAL GN
CLINICAL FEATURES
• young child, presenting with acute nephritic syndrome,
• having sudden and abrupt onset following an episode of sore throat or
skin infection
• microscopic or intermittent haematuria,
• red cell casts,
• mild non-selective proteinuria (less than 3 gm per 24 hrs),
• hypertension,
• periorbital oedema
• variably oliguria.
• In adults, the features are atypical and include sudden hypertension,
oedema and azotaemia.