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nephrotic & nephritic Flashcards

1
Q

nephrotic syndrome diseases

A

Minimal change disease, FOCAL SEGMENTAL GLOMERULOSCLEROSIS, Membranous GN

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2
Q

Nephritic Syndrome diseases

A

ACUTE DIFFUSE PROLIFERATIVE GN, RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS, IgA NEPHROPATHY, MEMBRANOPROLIFERATIVE GN

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3
Q

lipoid nephrosi

A

Minimal change disease

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4
Q

nil change disease

A

Minimal change disease

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5
Q

Minimal change disease etiology

A

Dysfunction of T-cells

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6
Q

Minimal change disease associated with

A

Podocytes Fusion (foot processes) of epithelial cells
Almost normal glomerulus by Light Microscope (LM)

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7
Q

Most common cause of Nephrotic Syndrome in children

A

Minimal change disease

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8
Q

Minimal change disease incidence in adults and children

A

10%, 65%

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9
Q

Minimal change disease age group

A

2-6 y 1w after uti or immunization

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10
Q

Minimal change disease distungsting feature

A

selective protinuria

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11
Q

Minimal change disease clinical course

A

selective proteinuria, normal renal function & respond to steroid

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12
Q

Minimal change disease labratory findingds

A

lm normal
if negative
em podocytes fusion

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13
Q

FOCAL SEGMENTAL GLOMERULOSCLEROSIS etiology

A

HIV, heroin addiction, obesity, SCd, glomerular scarring, maladaptation, inherited & primary disease

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14
Q

FOCAL SEGMENTAL GLOMERULOSCLEROSIS congenital forms:

A

mutations at APOL1 on ch.22 and increased risk of RF and FSGS, in africans
These mutations affect cytoskeletal or related proteins in podocytes (Nephrin)

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15
Q

FOCAL SEGMENTAL GLOMERULOSCLEROSIS lm

A

Collapse of BM
↑ mesangial matrix
Deposition of hyaline masses (hyalinosis)

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16
Q

FOCAL SEGMENTAL GLOMERULOSCLEROSIS em

A

Loss of podocytes.
Focal denudation of epithelial cells.

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17
Q

FOCAL SEGMENTAL GLOMERULOSCLEROSIS if

A

IgM & C3 deposition.

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18
Q

FOCAL SEGMENTAL GLOMERULOSCLEROSIS clinical

A

higher incidence of hematuria, ↓ GFR, & HT.
Nonselective proteinuria
poor response to steroids.

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19
Q

FOCAL SEGMENTAL GLOMERULOSCLEROSIS incidence

A

10% CHILDREN, 35% ADULTS

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20
Q

Membranous GN incidence

A

Adults 30%, children 5%

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21
Q

Membranous GN autoantibodies

A

M-type phospholipase A2 receptor–70% of the cases (important), Aldose reductase, Maganese superoxide dismutase 2,Membrane metalloendopeptidase.

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22
Q

Membranous GN most common autoantibodies

A

M-type phospholipase A2 receptor

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23
Q

Membranous GN prognosis

A

33% spontaneously remission.
33% stable with proteinuria.
33% progress to ESRD

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24
Q

Membranous GN LM

A

Thick capillary Wall without proliferation
Silver stain: spikes
wire loop lesion.

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25
Q

Membranous GN EM

A

Diffuse subepithelial deposits.

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26
Q

Membranous GN if

A

Granular IgG & C3 deposition.

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27
Q

Nephritic Syndrome manifestation

A

hematuria, htn, high blood urea, high serum creatinine, edema

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28
Q

Nephritic Syndrome pathogensis

A

Inflammatory lesions of glomeruli

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29
Q

Nephritic Syndrome clinical

A

Reduced GFR, htn, oliguria, fluid retention, and azotemia

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30
Q

ACUTE DIFFUSE PROLIFERATIVE GN etiology

A

1-4w after group a streptococcus b hemolytic infection

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31
Q

ACUTE DIFFUSE PROLIFERATIVE GN pathogensis

A

↑ ASO titer (Anti-streptolysin O)
Immune-complex disease/ Circulating or implanted Ag ↓ serum complement
Implicated Ags, SpeB, GAPDH, endostreptosin & plasmin binding protein

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32
Q

ACUTE DIFFUSE PROLIFERATIVE GN lm

A

Diffuse proliferation & leukocytic infiltration

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33
Q

ACUTE DIFFUSE PROLIFERATIVE GN em

A

subepithelial humps

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34
Q

ACUTE DIFFUSE PROLIFERATIVE IF

A

granular IgG & C3 in GBM and Mesangium

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35
Q

ACUTE DIFFUSE PROLIFERATIVE clinical

A

Gross hematuria & red casts; mild proteinuria

36
Q

ACUTE DIFFUSE PROLIFERATIVE children prognosis

A

> 95% recovery ,1% RPGN ,2% CRF

37
Q

ACUTE DIFFUSE PROLIFERATIVE adult prognosis

A

15-50% develop ESRD

38
Q

RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS types

A

Anti-GBM antibody–mediated crescentic GN
Pauci-immune type crescentic GN:
Immune-complex–mediated crescentic GN

39
Q

presence of crescents

A

RPGN

40
Q

Anti-GBM antibody–mediated crescentic GN if

A

Linear pattern for IgG & C3

41
Q

Anti-GBM antibody–mediated crescentic GN incidence

A

least common, 12%

42
Q

hemoptysis & hematouria

A

Good Pastus syndrome
Anti-GBM antibody–mediated crescentic

43
Q

Immune-complex–mediated crescentic GN IF

A

igG & c3

44
Q

Immune-complex–mediated crescentic GN incidence

A

44%

45
Q

Immune-complex–mediated crescentic GN seen in

A

Primary diseases (post-infect, IgA Nephtopathy)
Systemic (SLE, Henoch-Schoenlein purpura)
Idiopathic

46
Q

Pauci-immune type crescentic GN IF

A

negative

47
Q

Pauci-immune type crescentic GN incidence

A

44%

48
Q

ANCA

A

Pauci-immune type crescentic GN

49
Q

systemic vasculitis is associated with

A

Pauci-immune type crescentic GN

50
Q

rpgn lm

A

> 50-75% of glomeruli contain crescents
Some areas are still look good.
NL or focal proliferative changes.

51
Q

systemic vasculits types

A

Microscopic Polyangiitis
Granulomatosis with polyangiitis.

52
Q

rpgn em

A

rupture of GBM only or with electron-dense deposits

53
Q

rpgn prognosis

A

More than 80% bad prognosis

54
Q

rpgn therapy

A

steroid, cytotoxic, long term dialysis, renal transplant & Plasmapheresis

55
Q

Plasmapheresis used in

A

Anti-GBM and pauci-immune

56
Q

Commonest type of GN

A

IgA NEPHROPATHY

57
Q

IgA NEPHROPATHY incidence

A

10% children 15% adults

58
Q

IgA NEPHROPATHY etiology

A

1-2d after uti

59
Q

IgA NEPHROPATHY pathogensis

A

abnormality leading to ↑IgA synthesis after Antigenic stimulation, Circulating IgA aggregates or complexes entrapped in mesangium(have CD71), Activation of alternative pathway of complement

60
Q

Secondary IgA nephropathy

A

Celiac disease: ↑ IgA secretion due to mucosal inflammation
Liver disease: liver is responsible for clearance of IgA from.

61
Q

IgA nephropathy LM

A

Normal (initially) to focal or diffuse proliferative

62
Q

IgA nephropathy em

A

electron-dense deposits in the mesangium

63
Q

IgA nephropathy if

A

diffuse, usually global mesangial IgA in all cases

64
Q

IgA nephropathy prognosis

A

Initial benign course but slowly progressive
20-50% progress to CRF in 20 yrs
20 -60% recur in transplants.

65
Q

IgA nephropathy Bad prognostic features:

A

Old age
Heavy proteinuria
Associated HTN
Glomerular sclerosis

66
Q

MEMBRANOPROLIFERATIVE GN etiology

A

Chronic immune-complex disorder (SLE, HCV, HBV, HIV) Chronic bacterial infections, schistosomiasis
Malignant conditions (CLL, lymphoma, melanoma)

67
Q

MEMBRANOPROLIFERATIVE GN incidence

A

10% in both

68
Q

MEMBRANOPROLIFERATIVE GN principal presention

A

nephrotic sy, may begin as acute nephritis or mild proteinuria

69
Q

MPGN type 1 lm

A

tram-tracking (thickened reduplicated capillaries)
Tubulointerstitial changes & vascular changes of HTN.
Lobular accentuation
Enlarged glomeruli, proliferation + inflammatory infiltrate

70
Q

MPGN type 1 em

A

Subendothelial deposits
Circumferential mesangial interposition
Increase in mesangial cells & matrix.

71
Q

MPGN type 1 if

A

C3, C1q, C4 in granular pattern in mesangial area.

72
Q

mpgn occures in transplanr

A

Dense Deposit Disease

73
Q

Dense Deposit Disease

A

Abnormality that lead to activation of alternative pathway in the presence of C3 nephritic facto (Auto-Ab that stabilizes C3 convertase)
Normal C1 & C4, Low factor B & properdin

74
Q

Dense Deposit Disease LM

A

hypercellular glomeruli, duplicated BM & ↑ mesangial matrix

75
Q

Dense Deposit Disease em

A

Irregular, Ribbon like, extremely dense structure of the lamina densa & subepithelail space of the GBM

76
Q

Dense Deposit Disease if

A

Granular mesangial deposits
Short or discontinuous linear capillary loop deposits of C3.
No early complement components or Ig

77
Q

mpgn prognosis

A

40%: progress to ESRF
30%: variable degree of renal insufficiency
30%: persistent nephrotic S without RF.

78
Q

which worse prognosis mpgn 1 or ddd

A

ddd

79
Q

Alport syndrome clincal course

A

Ear (cochlea): nerve deafness
Eye (cornea): eye disorders.
Kidney (glomerulus): Nephritis

80
Q

Alport syndrome sex incidence

A

m>f

81
Q

HEREDITARY NEPHRITIS

A

Alport syndrome, THIN MEMBRANE DISEASE

82
Q

Alport syndrome lm

A

Secondary sclerosis later
Foam cells (histiocytes) in the interstitium.

83
Q

Alport syndrome em

A

GBM shows irregular thickening, lamination
splitting (“basketweave” appearance)

84
Q

Alport syndrome etiology

A

Mutation in encoding for alpha-5 chain of collagen type IV

85
Q

Alport syndrome prognosis

A

CRF in 20 yrs

86
Q

THIN MEMBRANE DISEASE etiology

A

Mutation in gene encoding alpha 3&4 chain of collagen type IV

87
Q

THIN MEMBRANE DISEASE prognosis

A

excellent, no systemic manifestation, no progression to rf

pathology (5 decks)

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