Renal Pathology Puthoff Lecture Flashcards Preview

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Flashcards in Renal Pathology Puthoff Lecture Deck (114)
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61

Primary Glomerulonephropathies

-Acute Proliferative Glomerulonephritis (usually DIFFUSE)
-RPGN
-Membranous Glomerulopathy
-Minimal change disease (lipoid necrosis/ mills disease)
-Focal Segmental glomerulosclerosis
-Membranoproliferative Glomerulonephritis (mesangial-capillary GN)--Dense deposit disease
-IgA nephropathy (acute FOCAL GN)
-Chronic Glomerulonephritis--End stage

62

Systemic diseases with glomerular involvement

-Lupus
-Diabetes

Not as common:
-Amyloidosis
-Goodpasture
-Microscopic polyarteritis/angiitis
-Wegener granulomatosis
-Henoch-schonlein purpura (IgA systemic disease!)
-Bacterial endocarditis

63

Systemic diseases with glomerular involvement--Heriditary disorders

-Alport syndrome
-Thin Basement membrane disease
-Fabry disease

64

Immune complexes in the glomerulus Subepithelial humps

acute glomerulonephritis

65

Immune complexes in the glomerulus--epimembranous depostis

Membranous nephropathy
Herman glomerulonephritis

66

Immune complexes in the glomerulus--SUBENDOTHELIAL DEPOSITS

Lupus nephritis
Membranoproliferazive glomerulonephritis

67

Immune complexes in the glomerulus--Mesangial deposits

--Acute focal proliferative GN!
-IgA nephropathy!!

68

Immune mechanisms of glomerular injury

-Ab mediated (in situ immune complex deposition)--fixed, intrinsic tissue Ags OR planted Ags
-Circulating immune complex deposition (Endogenous or exogenous Ags)
-Cell mediate immune injury
-Activation of alternative complement pathway

69

Ab mediated Glomerular injury

-deposition, circulating immune complexes sub endothelial
-In situ deposition on BM
-In situ deposition on foot processes--Heymann

70

Difference between Diffuse, focal, segmental and global

-diffuse involves all glomeruli
-Focal involves only subset of glomeruli
-Segmental means only portions of the affected glomeruli involved
-global means it involves entire glomerulus

71

Once GFR is reduced to 30-50% what happens?

-regadless of the stimulus underlying disease it results in FSGS and tubulointerstitial fibrosis even though it may not start as such

72

Proteinuria in nephrotic syndrome vs FSGS

-nephrotic is selective proteinuria--mostly just albumin
-FSGS is nonselective

73

Immune complex injury triggered by exogenous bacterial, viral or fungal Ag
Historically antecedent of Group A hemolytic stop; specific nephritogenic strains of Lacefield group A

Acute proliferative Glomerulonephritis

74

Diffuse proliferative glomerulonephritis characterized by

-marked hypercellularity: ranges from simple mesangial to complex endocapillary cell infiltrate
-Leukocyte infiltration: exudate within glomerular tuft

75

EM: sub epithelial hump of immune complex; neutrophil in lumen

Acute proliferative glomerulonephritis

76

Acute proliferative glomerulonephritis IF findings

Granular deposits of IgG, IgM, and C3 in mesangium and along the GBM corresponding to sub epithelial humps

77

Acute proliferative glomerulonephritis children clinical presentation

-ages 6-10
-typically 1-4 wks following pharyngitis or skin infection
-often but not invariably strep B
-often present with malaise, fever, nausea, oliguria, and hematuria 1-2 wks after recovery from sore throat; dysmorphic RBC cast, mild proteinuria (

78

Acute proliferative glomerulonephritis --adults clinical

-more typical and aggressive course
-may see sudden HTN or edema with elevated BUN

79

Acute proliferative glomerulonephritis children vs adults clinical course

-Children clear in 6-8 wks--renal biopsy not indicated
-95% recover completely;

80

Acute proliferative glomerulonephritis associated with what infections besides strep B?

-other bacterial (immunoglobulin feature with some staph infections)
-viral
-sequel to parasitic infx

81

What do you see in nephritic syndrome

-MAY exhibit nephritic syndrome with systemic disorders but typically seen in setting of post infectious disease and exudative GN, and syndromic clinical features helpful in dx of crescentic GN

82

Where do crescent formations occur?

-Bowmans space bw parietal (modified squamous cells) and visceral epithelial cells

83

Crescentic GN characteristic of what disorder?

-RPGN
-crescent shaped mass of proliferating visceral and parietal epithelial cells
-Rather rapid obliteration of urinary space
-infiltrates of macrophages & leukocytes
-PAS stain

84

RPGN Type 1

ANTI-GBM Ab
-Renal limited
-Goodpastures syndrome (kidney and lung hemorrhage)

85

RPGN Type 2

IMMUNE COMPLEX
-Idiopathic
-postinfectious GN
-Lupus nephritis
-Henoch Schönlein Purpura (systemic IgA disease)
-IgA nephropathy (renal limited IgA disease)
other

**Not all of these start out as RPGN!! They may be acute and focal and progress to RPGN later

86

Type 3 RPGN

PAUCI IMMUNE
-ANCA associated (anti neutrophil cytoplasmic associated)
-Idiopathic
-Granulomatosis with polyangiitis--wegners associated with ANCA
-Microscopic polyangiitis

87

50% of PRIMARY renal diseases (so not lupus or Heoch schnolen bc these are systemic) associated with RPGN have what type of RPGN on IF

Type III (paci immune) on IF

88

Type I RPGN characterized by

-anti-GBM Ab-induced disease characterized by LINEAR deposits of IgG and many cases C3 in GBM

89

What happens when anti GBM Abs cross react with lung alveolar BM?

Pulmonary hemorrhage occurs in addition to renal disease (Goodpassure's syndrome)

90

Good pasture Ag is a
IF pattern

peptide within non collagenous regions of collagen type IV
-Anti-IgG localized to glomerular BM with DIFFUSE LINEAR staining