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Amyloidosis 1.

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Presentation on theme: "Amyloidosis 1."— Presentation transcript:

1 Amyloidosis 1

2 Amyloidosis of the kidney
2

3 LM EM IF Disease MPGN Focal GN Amyloidosis DM Membranous GN
Thickened GBM Subepithelial Deposits Granular fl.of GBM MPGN Minimal change Focal and Seg.GS Focal GN Lupus Nephritis Amyloidosis DM 3

4 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. 4

5 Chronic GN: Note contracted kidney& granular outer surface
5

6 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 6

7 Chronic glomerulonephritis
7

8 Chronic GN Hyaline cast 8

9 9

10 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 10

11 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). 11

12 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. 12

13 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 13

14 Diffuse glomeruosclerosis
14

15 15

16 Nodular GS 16

17 Nodular GS 17

18 18

19 Fibrin cap and Capsular drop
19

20 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. 20

21 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. 21

22 Proliferative lupus nephritis Flea-Bitten appearance
22

23 Class II: Mesangial GN 23

24 Focal and segmental necrosis of glomerulus
Class III: Focal GN Focal and segmental necrosis of glomerulus 24

25 Class IV:Diffuse Proliferaive GN
Hematoxylin bodies Wire-Loop appearance 25

26 IF of Lupus Nephritis 26

27 EM of Lupus Nephritis 27

28 IF: Granular fluorescence of capillary walls for Igs and comploments
EM: Subendothelial and mesangial electron dense deposits 28

29 Tubulointerstitial nephritis
Def: diseases affecting tubules and interstitial tissues of the kidney. 1-Pyelonephritis Pelvis of the kidney is commonly involved in bacterial infection,hence pyelo Cause: bacterial infection as E-coli ,B. proteus, B. pyocyaneus and others PF: -obstruction Vesicoureteric reflux -Instrumentation Female sex. -Pregnancy DM. -Bilhaziasis.

30

31 Acute PN Routes of infection Grossly: Hematogenous -Ascending
From boil -Ascending Lymphatic from GIT Acute PN Grossly: -Enlarged kidney Congested PCS -Yellow streaks from papillae to cortex.

32 Acute PN

33 Yellow foci of pus

34 Acute pyelonephritis

35 Chronic PN Gross Characterized by:
-Interstitial inflammation and scarring -Deformity andscarring of pelvicalyceal system Gross -Small sized kidney (contracted). -Irregular outer surface due to retraction of the capsule. -Distorted pelvicalceal system .

36 Chronic pyelonephritis

37 Chronic PN

38 Microscopic: -Periglomerular fibrosis
-Dilated tubules containing hyaline casts (thyrodization) -Thick walled BVs -Interstitial fibrosis and chronic inflammatory cell infiltration.

39 Microscopic of Ch.PN

40 Chronic PN. Note periglomerular fibrosis

41 Ch. PN. Thyrodization

42 Complication -Secondary hypertension. -proteinuria. -Chronic renal failure.

43 Other types of renal infection
-Pyaemia -Tuberculosis.

44 2-Drug-induced interstitial nephritis Mechanisms:
1-immunologic reaction or hypersensitivity reaction type I Acute interstitial nephritis e.g rifampicin, penicellin,thiazides 2-Slow damage to tubules Chronic interstitial nephritis via type IV reaction e.g. Analgesic nephropathy 3-Direct nephrotoxicity ATN

45 Drug induced interstitial nephritis

46 Chronic tubulointerstitial nephritis

47 3-Acute tubular necrosis
Def: destruction of tubular epithelial cells with acute suppression of kidney function. It is reversible renal lesion. Types Toxic ATN -poisons as Mgcl, CCl4,Phosphorus, &insecticides -Drugs e.g. gentam ,amphotricin B Anoxic(ischemic) ATN: -Mismatched biood trasfusion -Shock &severe hypotension -Severe trauma

48 Acute tubular necrosis

49 Acute tubular necrosis

50 Vascular diseases of the kidney 1-Renal artery stenosis
Cause:-Atheromatous plaque. -Fibromuscular dysplasia. Effects: secondary hypertension(2-5%),due to renin production. 2-Infarcts Presented by painless hematuria. Causes:-Embolism Thrombosis on top AS

51 Atheromatous plaque

52 Thrombosed renal artery

53 Infarct of the Kidney

54 Infact kidney

55 Infarction of The kidney

56 3-Senile atherosclerotic kidney
Grossly: -Both kidneys are reduced in size. -The outer surfaces show depressions due to scarring -The renal artery is atheromatous. MSC: -Wedge-shaped areas of fibrosis. -Hyalinized glomeruli. - Tubules.are replaced by fibrous tissue

57 Atherosc.of the aorta and kidneys

58 Aortic Aneurysm with thrombus and senile kidneys

59 Atherosclerotic kidney
Atherosclerotic renal artery Atherosclerotic kidney

60 Atheromatous plaque

61 A-Benign nephrosclerosis
4-Hypertension A-Benign nephrosclerosis Microscopic; -Hyaline arteriolosclerosis -Fibroelastic hyperplasia of large arteries -Diffuse ischemic atrophy of the nephron Grossly; -Both kidneys are reduced in size (contracted) -Granular outer surface -Loss of demarcation between cortex and medulla

62 B. Nephrosclerosis

63 Arteiolosclerotic kidney

64 Arteriolonephrosclerosis

65 Benign nephrosclerosis

66 Benign Nephrosclerosis

67

68 B-Malignant nephrosclerosis
Microscopic: -Fibrinoid necrosis -Smooth muscle proliferation and duplication of basement membrane ( onion-skin appearance) -Necrotizing glomerulitis Grossly: -Enlarged kidney with peticheal he

69 Fibrinoid necrosis in malignant hypertension

70 Malig. Nephrosclerosis. Onion –skin appearance

71 5-Bilateral cortical necrosis 6-Necrosis of renal papillae
Rare lesion Cause; ischemic as in toxemia of pregnancy or severe infections such as pneumonias and diphtherias Gross; yellow cortex of both kidneys MSC: Coagulative necrosis 6-Necrosis of renal papillae Cause :ischemic necrosis due to PN, with DM, excess phenacetin and chronic alcoholism

72 Cortical necrosis

73 Necrosis of renal papillae

74 Necrotizing papillitis

75 Necrosis of renal papillae


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