Patholog -Neutrophils infiltration secoed Hnioeudiy Ousia WBC WBC e g 停 magnification x 1000. h&e stain marked influx of polymorphonuclear leukocytes(arrows)
magnification ×1000, H&E stain , marked influx of polymorphonuclear leukocytes(arrows) Pathology ◼Neutrophils infiltration WBC WBC WBC
Immunofluorescence in Second tatiooadidy oleat Granular deposits lumpy- bumpy deposits of immunoglobulin and complement on the glomerular basement membranes and in the mesangium
Immunofluorescence Granular deposits lumpy - bumpy deposits of immunoglobulin and complement on the glomerular basement membranes and in the mesangium
Subepithelial "lumps immune compleXes deposition Electron mIcroscopy
Subepithelial “lumps” immune complexes deposition Electron microscopy
3. Pathophysiology beta hemolytic streptococci (Ag) Form cic or IC Glomerular local inflammation Endocapillary proliferation GBM damage GRF↓ Hematuria and Water and salt retention oliguria proteinuria Edema severe congestion of circulation or和 Extra celluar fluid volume t hypertension hypertensive encephalopathy
3.Pathophysiology Form CIC or IC Glomerular local inflammation Endocapillary proliferation GBM damage GRF↓ Water and salt rotention oilguria Extra celluar fluid volume ↑ Edema hypertension severe congestion of circulation or 和 hypertensive encephalopathy Hematuria and proteinuria beta hemolytic streptococci （Ag）
4. Clinical manifestation osa Sat tiny us K Atypical patients Asymptomatic( occasionally hematuria with/without proteinuria ◆ Nephrotic syndrome ◆ extrarenal|form Typical patients Acute nephritic syndrome Severe patients severe congestion of circulation Hypertensive encephalopathy ◆ Acute renal failure
4.Clinical manifestation ➢ Atypical patients ♦ Asymptomatic( occasionally hematuria with/without proteinuria ♦ Nephrotic syndrome ♦ extrarenal form ➢ Typical patients ♦ Acute nephritic syndrome ➢ Severe patients ♦ severe congestion of circulation ♦ Hypertensive encephalopathy ♦ Acute renal failure