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nephrotic & nephritic Flashcards

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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
Membranous GN EM
Diffuse subepithelial deposits.
26
Membranous GN if
Granular IgG & C3 deposition.
27
Nephritic Syndrome manifestation
hematuria, htn, high blood urea, high serum creatinine, edema
28
Nephritic Syndrome pathogensis
Inflammatory lesions of glomeruli
29
Nephritic Syndrome clinical
Reduced GFR, htn, oliguria, fluid retention, and azotemia
30
ACUTE DIFFUSE PROLIFERATIVE GN etiology
1-4w after group a streptococcus b hemolytic infection
31
ACUTE DIFFUSE PROLIFERATIVE GN pathogensis
↑ ASO titer (Anti-streptolysin O) Immune-complex disease/ Circulating or implanted Ag ↓ serum complement Implicated Ags, SpeB, GAPDH, endostreptosin & plasmin binding protein
32
ACUTE DIFFUSE PROLIFERATIVE GN lm
Diffuse proliferation & leukocytic infiltration
33
ACUTE DIFFUSE PROLIFERATIVE GN em
subepithelial humps
34
ACUTE DIFFUSE PROLIFERATIVE IF
granular IgG & C3 in GBM and Mesangium
35
ACUTE DIFFUSE PROLIFERATIVE clinical
Gross hematuria & red casts; mild proteinuria
36
ACUTE DIFFUSE PROLIFERATIVE children prognosis
>95% recovery ,1% RPGN ,2% CRF
37
ACUTE DIFFUSE PROLIFERATIVE adult prognosis
15-50% develop ESRD
38
RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS types
Anti-GBM antibody–mediated crescentic GN Pauci-immune type crescentic GN: Immune-complex–mediated crescentic GN
39
presence of crescents
RPGN
40
Anti-GBM antibody–mediated crescentic GN if
Linear pattern for IgG & C3
41
Anti-GBM antibody–mediated crescentic GN incidence
least common, 12%
42
hemoptysis & hematouria
Good Pastus syndrome Anti-GBM antibody–mediated crescentic
43
Immune-complex–mediated crescentic GN IF
igG & c3
44
Immune-complex–mediated crescentic GN incidence
44%
45
Immune-complex–mediated crescentic GN seen in
Primary diseases (post-infect, IgA Nephtopathy) Systemic (SLE, Henoch-Schoenlein purpura) Idiopathic
46
Pauci-immune type crescentic GN IF
negative
47
Pauci-immune type crescentic GN incidence
44%
48
ANCA
Pauci-immune type crescentic GN
49
systemic vasculitis is associated with
Pauci-immune type crescentic GN
50
rpgn lm
> 50-75% of glomeruli contain crescents Some areas are still look good. NL or focal proliferative changes.
51
systemic vasculits types
Microscopic Polyangiitis Granulomatosis with polyangiitis.
52
rpgn em
rupture of GBM only or with electron-dense deposits
53
rpgn prognosis
More than 80% bad prognosis
54
rpgn therapy
steroid, cytotoxic, long term dialysis, renal transplant & Plasmapheresis
55
Plasmapheresis used in
Anti-GBM and pauci-immune
56
Commonest type of GN
IgA NEPHROPATHY
57
IgA NEPHROPATHY incidence
10% children 15% adults
58
IgA NEPHROPATHY etiology
1-2d after uti
59
IgA NEPHROPATHY pathogensis
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
Secondary IgA nephropathy
Celiac disease: ↑ IgA secretion due to mucosal inflammation Liver disease: liver is responsible for clearance of IgA from.
61
IgA nephropathy LM
Normal (initially) to focal or diffuse proliferative
62
IgA nephropathy em
electron-dense deposits in the mesangium
63
IgA nephropathy if
diffuse, usually global mesangial IgA in all cases
64
IgA nephropathy prognosis
Initial benign course but slowly progressive 20-50% progress to CRF in 20 yrs 20 -60% recur in transplants.
65
IgA nephropathy Bad prognostic features:
Old age Heavy proteinuria Associated HTN Glomerular sclerosis
66
MEMBRANOPROLIFERATIVE GN etiology
Chronic immune-complex disorder (SLE, HCV, HBV, HIV) Chronic bacterial infections, schistosomiasis Malignant conditions (CLL, lymphoma, melanoma)
67
MEMBRANOPROLIFERATIVE GN incidence
10% in both
68
MEMBRANOPROLIFERATIVE GN principal presention
nephrotic sy, may begin as acute nephritis or mild proteinuria
69
MPGN type 1 lm
tram-tracking (thickened reduplicated capillaries) Tubulointerstitial changes & vascular changes of HTN. Lobular accentuation Enlarged glomeruli, proliferation + inflammatory infiltrate
70
MPGN type 1 em
Subendothelial deposits Circumferential mesangial interposition Increase in mesangial cells & matrix.
71
MPGN type 1 if
C3, C1q, C4 in granular pattern in mesangial area.
72
mpgn occures in transplanr
Dense Deposit Disease
73
Dense Deposit Disease
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
Dense Deposit Disease LM
hypercellular glomeruli, duplicated BM & ↑ mesangial matrix
75
Dense Deposit Disease em
Irregular, Ribbon like, extremely dense structure of the lamina densa & subepithelail space of the GBM
76
Dense Deposit Disease if
Granular mesangial deposits Short or discontinuous linear capillary loop deposits of C3. No early complement components or Ig
77
mpgn prognosis
40%: progress to ESRF 30%: variable degree of renal insufficiency 30%: persistent nephrotic S without RF.
78
which worse prognosis mpgn 1 or ddd
ddd
79
Alport syndrome clincal course
Ear (cochlea): nerve deafness Eye (cornea): eye disorders. Kidney (glomerulus): Nephritis
80
Alport syndrome sex incidence
m>f
81
HEREDITARY NEPHRITIS
Alport syndrome, THIN MEMBRANE DISEASE
82
Alport syndrome lm
Secondary sclerosis later Foam cells (histiocytes) in the interstitium.
83
Alport syndrome em
GBM shows irregular thickening, lamination splitting (“basketweave” appearance)
84
Alport syndrome etiology
Mutation in encoding for alpha-5 chain of collagen type IV
85
Alport syndrome prognosis
CRF in 20 yrs
86
THIN MEMBRANE DISEASE etiology
Mutation in gene encoding alpha 3&4 chain of collagen type IV
87
THIN MEMBRANE DISEASE prognosis
excellent, no systemic manifestation, no progression to rf

pathology (5 decks)

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