1. The nephrotic syndrome
Def: It is a clinico -biochemical state of many causes
Features
1-Heavy proteinuria.
2-Hypoproteinemia.( decrease protein in the blood)
3-Generalized oedema.
4-Hyperlipidemia and lipiduria

2. Causes Systemic Diseases Renal 1-SLE 1-Membranous GN 2-DM
3-Amyloidosis
4-Infections e.g.; malaria, HBV,B
Syphilis
6-lymphoma
7-Drugs:gold salt and NSAI
Renal
1-Membranous GN
2-membranoproliferative GN
3-Minimal change GN
4-Focal segmental GS
5-Focal GN.(Mesangial,IgA
Nephropathy)

3. Common features of nephrotic syndrome
Gross
-Enlarged pale kidney.
-yellow ting due to fat resorption by
tubular epithelium.

4. Microscopic 1-Glomeruli; LM&IF: Features specific to the disease.
EM: Fusion of foot processes of podocytes.
2-Tubules
1-Hyaline droplets.
2-Vacuolar degeneration due to resorption of fat
3-Hyaline casts
3-Interstitial tissue
variable oedema

6. Hyaline casts

7. Membranous GN Age: adults (30-50 ys) Patho: ICD Cause:-
-Primary :Unknown (85%)
-Secondary in course of infection like malaria syphilis, HBV, B, malignant tumors and gold salt therapy
Patho: ICD

8. Microscopic Light: IF Thickening of the GBM Granular EM:
flourescences to IgG and C3
EM:
-Fusion of foot processes
Of podocytes.
-Subepithelial deposits

9. Thickened GBM IN MGN

10. Sikes formation in MGN. Silver stain

11. Spikes formation along GBM
Silver stain

12. Diffuse granular fluorescence of GBM

13. EM in MGN, the darker electron dense immune deposits are seen scattered within the thickened basement membrane.

14. Membranous GN.EM
Subepithelial Deposits

15. Prognosis: Remission and exacerbation, finally chronic renal failure.
Clinical and laboratory findings Nephrotic syndrome
Prognosis: Remission and exacerbation, finally chronic renal failure.

16. Minimal change GN Msc:1-Light Gross: as Nephrotic syndrome.
Age: Commonest cause of nephrotic syndrome in children (1-4 ys )
Pathog: unknown or it is a disorder of T cells
cytokines that cause loss of epithelial foot processes
Gross: as Nephrotic syndrome.
Msc:1-Light
Glomeruli ; no changes.

18. 2-IF: Negative. 3-EM: Fusion of foot processes of podocytes
Tubules and interstitial tissues show changes of nephrotic syndrome
2-IF: Negative.
3-EM: Fusion of foot processes of podocytes
Clinical and laboratory findings : as NS with selective proteinuria.
Prognosis: good response to steroid therapy

20. Membranoproliferative GN
Age; any age, mainly late childhood
Pathogenesis;
Type I; Common. It is ICD
Type II (Dense deposit disease) :rare mediated by activation of the alternative complement pathway.

21. Accentuated lobulation Patchy irregular thickening of GBM
MSC;1-Light
Hypercellularity
Double contour of GBM
Accentuated lobulation
Patchy irregular thickening of GBM

22. MPGN, the glomerulus has increased overall cellularity, mainly mesangial

23. MPGN.Lobulation. Patchy irregular Thickening of GBM

24. New matrix material is laid down resulting in replication of basement membrane material

25. Membranoproliferative GN type I

26. This silver stain demonstrates a double contour to many basement membranes, or the "tram-tracking" that is characteristic of MPGN

27. 2-IF; Type I: Gr.fluor.to Igs and C3

28. Bright deposits in type II MPGN To C3

29. TYPE II, intramembranous deposit

30. Clinical and laboratory findings
Presentation
Asymptomatic proteinuria
Nephrotic syndome+ hypertension
Nephritic syndrome
Prognosis : remission exacerbation and finally chronic renal failure

31. Focal segmental glomerulosclerosis
Microscopic: -Sclerotic segments in some gl. and
Hyalinosis
-tubular atrophy
-interstitial fibrosis
IF: Granular fluorescence of the GBM for IgM andC3.
EM:Fusion of foot processes and detachement of epithelial cells

32. Focal segmental GS

36. Clinically: Nephrotic syndrome, may be hypertension and microscopic hematuria.
Prognosis: unfavorable (ending in chronic renal failure

37. Focal glomerulonephritis
Cause: idiopathic
-In association of SBE,SLE, Henoch-schonlein PAN, and Goodpasture’s syndrome
Pathogenesis: -ICD
-Activation of the alternative complement pathway by aggregation of IgA.(Berger’s disease)

38. IgA Nephropathy (Berger’s Disease)
-Common in children and young adults
- Recurrent hematuria
-It follows infection of the respiratory,GI and urinary tracts.
-The IgA is deposited mainly in mesangium, which then increases mesangial cellularity

39. MSC: Focal and segmental proliferation of mesangial cells+ necrosis and crescent formation
Clinically: Hematuria, proteinuria and may be nephrotic syndrome
Course: Subsides without residual renal impairment

40. Focal glomerulonephritis
IF:Granular

41. Focal GN
Necrosis

42. Amyloidosis

43. Amyloidosis of the kidney

44. LM EM IF MPGN Minimal change Focal and Seg.GS Focal GN Lupus Nephritis
Disease LM EM IF
Membranous GN
MPGN
Minimal change
Focal and
Seg.GS
Focal GN
Lupus Nephritis

45. Chronic GN Grossly:-Small contracted kidney.
Def: it is end stage renal glomerular disease.
Grossly:-Small contracted kidney.
-Granular outer surface.
-Firmly adherent capsule.
-Loss of differentiation bet. cortex and medulla.
-Thick BVs at corticomedullary junction.

46. Chronic GN: Note contacted kidney& granular outer surface

47. Msc: Glomeruli: -Hyalinised and sclerotic. Tubules are atrophied and
-Some are hypertrophied.
Tubules are atrophied and
dilated
Interstitial fibrosis and chronic inflammatory cell infiltration
Thick walle-blood vessels
end arteritis obliterans

48. Chronic glomerulonephritis

49. Chronic GN
Hyaline cast

51. Clinical and laboratory Findings: Prognosis: without Treatment is poor
Urine changes
-Polyuria.
low Specific gra.
-Mild albuminuria.
-Hyaline and
granular casts
Marked
hypertension
Increase
Bl. urea
Prognosis: without Treatment is poor

52. Small- Sized Kidney (contracted kidney)
1-Hypoplastic kidney.
2-Chronic GN
3-Chronic PN
4-Senile(atherosclerotic) kidney.
5-Kidney of benign hypertension (Benign nephrosclerosis).

53. DM Effects of DM on the kidney: -Diabetic GS
-Renal arteriolar sclerosis.
-pyelonephritis.
-papillary necrosis.
Diabetic GS
It leads to:
a-Proteinuria.
B-Nephrotic syndrome.
C-CRF.

54. MSC: 1-Diffuse GS. -Diffuse increase in mesangial matrix
-Thickening of GBM
2-Nodular GS. (kimmelsteil Wilson disease)
Hyaline nodule is present in the mesangium,
Containing fibrin and lipid.
3-Insudative lesion:
-fibrin cap; eosinophilic focal Thickening of
peripheral capillary loop.
-Capsular drop: eosinophilic thickening of
Bowman’s capsule

55. Diffuse glomeruosclerosis

57. Nodular GS

58. Nodular GS

60. Fibrin cap and Capsular drop

61. Lupus nephritis Classification;
Presentation: Recurrent hematuria,nephritic s,nephrotic s,hypertension,CRF.
Classification;
-class I:Normal kidney.
-Class II:Mesangial glomerular lesion.
-Class III:Focal proliferaive GN.
-Class IV:Diffuse Proliferative GN.
-Class V:Membranous GN.
-Class VI:Advancing sclerosing GN.

62. MSC of Class IV: Diffuse Proliferative GN
-Diffuse hypercellularity due to Proliferation of endothelial cells and mesangial cells Irregular thickening of GBM
- Wire loop appearance
-Few epith.crescents
-Hematoxylin bodies.

63. Proliferative lupus nephritis Flea-Bitten appearance

64. Class II: Mesangial GN

65. Focal and segmental necrosis of glomerulus
Class III: Focal GN
Focal and segmental necrosis of glomerulus

66. Class IV:Diffuse Proliferaive GN
Hematoxylin bodies
Wire-Loop appearance

67. IF of Lupus Nephritis

68. EM of Lupus Nephritis

69. IF: Granular fluorescence of capillary walls for Igs and comploments
EM: Subendothelial and mesangial electron dense deposits