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Glomerulonephritis Dr. Abdelaty Shawky Dr. Gehan mohamed.

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Presentation on theme: "Glomerulonephritis Dr. Abdelaty Shawky Dr. Gehan mohamed."— Presentation transcript:

1 Glomerulonephritis Dr. Abdelaty Shawky Dr. Gehan mohamed

2 Glomerular diseases constitute some of the major problems in nephrology; indeed, chronic glomerulonephritis is one of the most common causes of chronic renal failure in humans. Glomeruli may be injured by a variety of factors and in the course of a number of systemic diseases. Systemic immunologic diseases such as systemic lupus erythematosus (SLE), hypertension and polyarteritis nodosa, diabetes mellitus, often affect the glomerulus. These are termed secondary glomerular diseases to differentiate them from disorders in which the kidney is the only or predominant organ involved. 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. Rapidaly 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 haemorrhages. 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 Post-streptococcal GN 23

24 Post-streptococcal GN 24

25 * IF (Immunoflurescence): Deposition of Ig G and C3. 25

26 Positive Ig G and C3 26

27 * EM (Electron microscope): Subepithelial immune complex deposit (humps). 27

28 28

29 * CP (Clinical picture): In the classic case, a young child abruptly develops malaise, fever, nausea, oliguria, and hematuria (smoky or cocoa-colored urine) 1 to 2 weeks after recovery from a sore throat. The patients exhibit red cell casts in the urine, mild proteinuria (usually less than 1 mg/day), peri-orbital edema, and mild to moderate hypertension. 29

30 RBCs cast Hematuria (coca cola colored urine) 30

31 In adults, the onset is more likely to be atypical, with the sudden appearance of hypertension or edema, frequently with elevation of serum creatinine. Important laboratory findings include elevations of anti-streptococcal antibody (ASO) titers and a decline in the serum concentration of C3 (consumed). 31

32 More than 95% of affected children eventually recover totally with conservative therapy aimed at maintaining sodium and water balance. 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. 32

33 In adults, the prognosis is bad. Most of the patients pass to rapidly progressive glomerulonephritis or chronic renal failure. 33

34 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. 34

35 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. 35

36 Thanks 36 References: Robbins and Cotran’s: Pathologic Basis of Disease. Seventh edition.

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