1. Glomerulonephritis By Dr. Abdelaty Shawky Associate professor of pathology

2. Glomerular diseases constitute one of the major problems in nephrology; indeed, chronic glomerulonephritis is one of the most common causes of chronic renal failure in humans. 2

3. * Classification of glomerular diseases: I. Primary G.N (the disease affects kidney only): Minimal change glomerular disease (Lipoid nephrosis). Acute diffuse proliferative G.N: – Post-streptococcal G.N. – Non-post-streptococcal GN. Rapidly progressive G.N. Membraneous G.N. Membranoproliferative G.N. Chronic G.N. 3

4. II. Secondary G.N (the disease affects kidney and other organs): – Systemic lupus erythematosus (SLE). – Polyarteritis nodosa (PAN). – Wegener granulomatosis. – Diabetes mellitus (diabeteic nephropathy). – Goodpasture syndrome. – Amyloidosis. 4

5. Normal Glomerulus 5

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8. Most of the 1ry glomerular disease are due to immunologic mechanisms. To study any glomerular disease, a renal biopsy is taken and examined by 3 types of microscopes: 1. Light microscope: to examine the structure of glomeruli, tubules and interstitium. 2. IF (immune flourescent microscope): to detect the type of deposited immunoglobulin in the glomeruli. 3. EM (electron microscope): to detect the site of immune complex, either sub-epithelial, sub- endothelial, mesangial or basement membrane.. 8

9. Minimal change glomerular disease Minimal change glomerular disease 9

10. *Etiology & pathogenesis: Chemical change in the glomerular basement membrane causing protein loss. 10

11. * Grossly: Mild bilateral kidney enlargement. * LM (Light microscope): No abnormalities. * IF (Immunoflurescence): No immune deposits. * EM (Electron microscope): Fusion of the foot processes of the epithelial cells (podocytes). 11

12. EM of normal glomerulus 12

13. EM of minimal change glom. disease 13

14. * CP (Clinical picture): Affect children and young adults. Cause nephrotic syndrome. * Fate: The disease has excellent prognosis and most patients respond to corticosteroids with complete resolution of proteinuria. 14

15. Post-streptococcal G.N 15

16. *Etiology & pathogenesis: Immune complex reaction; (nephrotegenic strains of group A beta haemolytic streptococci + Ig G), the complex is deposited in the glomeruli with subsequent complement activation  acute inflammation. 16

17. * Grossly: Mild bilateral kidney enlargement with petechial hemorrhages. 17

18. * LM (Light microscope): a. Glomeruli: Proliferation of endothelial and mesangial cells. Glomerular capillaries contain neutrophils. Bowman’s space shows: neutrophils, RBCs, some albumin. b. Tubules: The lining cells are swollen. The lumens show casts (RBCs casts, neutrophil casts & hyaline casts). c. Interstitium: Acute inflammatory reaction…... 18

19. Normal kidney 19

20. Normal kidney 20

21. Post-streptococcal GN 21

22. Post-streptococcal GN 22

23. * IF (Immunoflurescence): Deposition of Ig G and C3. 23

24. Positive Ig G and C3 24

25. * EM (Electron microscope): Subepithelial immune complex deposit (humps). 25

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27. * CP (Clinical picture): A young child presents with oliguria, hematuria (cocoa-colored urine) and peri-orbital edema about 2 weeks after recovery from a sore throat. 27

28. RBCs cast Hematuria (coca cola colored urine) 28

29. More than 95% of the affected children eventually recover totally with treatment. A small minority of children (perhaps less than 1%) do not improve, become severely oliguric, and develop a rapidly progressive glomerulonephritis. Some of the remaining patients may undergo slow progression to chronic glomerulonephritis. 29

30. Nephritic syndrome - A syndrome formed of: 1. Haematuria. 2. Oliguria. 3. Peri-orbital oedema. 4. Hypertension. - The most common cause of nephritic syndrome in children is post-streptococcal GN. 30

31. Nephrotic syndrome - A syndrome formed of: 1. Hypoproteinaemia. 2. Proteinuria. 3. Oedema. 4. Hypercholesterolaemia. -The most common cause of nephrotic syndrome in children is minimal change glomerular disease. -The most common cause of nephrotic syndrome in adults is membranous GN. 31

32. 32 References: Robbins and Cotran’s: Pathologic Basis of Disease. Seventh edition. Thanks