7. Diagrams depicting the ultrastructural features of a normal glomerular capillary loop (A) , and the ultrastructural features of APSGN ( B ), Note the subepithelial hump like dense deposits and endocapillary hypercellularity.

9. IF micrograph of a glomerular segment from a patient with APSGN showing coarsely granular capillary wall staining for IgG(left) and C3(right). IgG and C3 deposition

10. EM of a portion of a glomerular capillary from a patient with APSGN showing subepithelial dense deposits and a neutrophil (N) marginated against the basement membrane with no intervening endothelial cytoplasm.

11. Immune complexes, antigens Activation of Compliments Recruitment of leukocytes GBM damage, Blood ingredients leakage Hematuria Proteinuria RBC Casts Proliferation of MC and EC Blockage of renal capillaries and decreased GFR Edema hypertention heart failure encephalopathy renal failure Oliguria, sodium and water retention, hypervolemia Inflammation mediates, Cytokines, proliferative F. Infection of streptocacci PATHOGENESIS

26. Clinical manifestations APSGN IgAN Goodpature Syndrome RPGN Age and sex All ages, 2 : 1 male 10–35 yr, 2 : 1 male 15–30 yr, 6 : 1 male Adults, 2 : 1 male nephritic syndrome 90% 50% 90% 90% Asymptomatic hematuria Occasionally 50% Rare Rare NS 10–20% Rare Rare 10–20% Hypertension 70% 30–50% Rare 25% ARF 50% (transient) Very rare 50% 60% Other Latent period of 1–3 wk Follows viral syndromes P. Hemorrhage IDA None Laboratory findings ↑ ASO titers (70%) ,↓C3 ↑ Serum IgA (50%) anti-GBM Ab Positive ANCA in some Renal pathology LM, IF Diffuse proliferation Granular IgG, C3 Focal proliferation Diffuse mesangial IgA deposits Focal ➙ diffuse Proliferation with crescents Linear IgG, C3 Crescentic GN No immune deposits Prognosis 95% resolve spontaneously 5% RPGN Slow progression in 25–50% 75% stabilize or improve if treated early 75% stabilize or improve if treated early

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