All glomeruli appear enlarged and relatively bloodless and show diffuse mesangial cell proliferation with an increase in mesangial matrix.
Polymorphonuclear leukocytes are common in glomeruli during the early stage of the disease.
Crescents and interstitial inflammation may be seen in severe cases.
IFM reveals lumpy-bumpy deposits of immunoglobulin and complement on the glomerular basement membrane (GBM) and in the mesangium.
EM: electron-dense deposits, or “humps,” are observed on the epithelial side of the GBM
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. A B
LM of a glomerulus with APSGN demonstrating marked influx of neutrophils (arrows). (Masson trichrome, ×700.)
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
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.
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
Although morphologic studies and a depression in the serum complement (C3) level strongly suggest that APSGN is mediated by immune complexes , the precise mechanisms by which nephritogenic streptococci induce complex formation remain to be determined.
The finding of circulating immune complexes in APSGN is not uniform
Complement activation is primarily through the alternative rather than the classic (immune complex–activated) pathway.
Spontaneous improvement typically begins within 1 wk with resolution of edema in 5-10 days and hypertension in 2-3 wk, but urinalysis may be abnormal ( persistent microscopic hematuria ) for several years.
75% stabilize or improve if treated early 75% stabilize or improve if treated early Slow progression in 25–50% 95% resolve spontaneously 5% RPGN Prognosis Crescentic GN No immune deposits Focal ➙ diffuse Proliferation with crescents Linear IgG, C3 Focal proliferation Diffuse mesangial IgA deposits Diffuse proliferation Granular IgG, C3 Renal pathology LM, IF Positive ANCA in some anti-GBM Ab ↑ Serum IgA (50%) ↑ ASO titers (70%) ,↓C3 Laboratory findings None P. Hemorrhage IDA Follows viral syndromes Latent period of 1–3 wk Other/Antecedent infection 60% 50% Very rare 50% (transient) ARF 25% Rare 30–50% 70% Hypertension 10–20% Rare Rare 10–20% NS Rare Rare 50% Occasionally Asymptomatic hematuria 90% 90% 50% 90% nephritic syndrome Adults, 2 : 1 male 15–30 yr, 6 : 1 male 10–35 yr, 2 : 1 male 5-12yr, rare<2 yr, 2 : 1 male Age and sex RPGN Goodpature Syndrome IgAN APSGN Clinical manifestations