3.7.3 Path: Nephritic Syndrome Flashcards

1
Q

Acute renal failure

A

Pre-renal: Shock or HF caused by MI
Renal: Glomerular destruction, Glomerulonephritis
Post renal: Sudden obstruction to urine outflow

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2
Q

EM findings of Acute Post-Infectious Glomerulonephritis

A

Subepithelial dense deposits that are shaped like humps on the epithelial side of the BM that are deposits of immune complexes

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3
Q

IF findings of Acute post infectious glomerulonephritis

A

Granular or “Lumpy-bumpy”deposits are both IgG and complement along the BM

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4
Q

Rapidly Progressive (Crescentic) GMN

A

Severe glomerular injury accompanied by formation of epithelial crescents in urinary space.

Inflammatory cells surround the compressed capillary loops in the form of crescent moon

Happens after focal necrosis of the glomerular capillaries in diseases such as goodpastures syndrome

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5
Q

Goodpasture syndrome

A

AI disease. Antibodies formed against collagen type 4.

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6
Q

Hallmark of Goodpasture syndrome

A

Diffuse linear staining of GBM for IgG–>Autoantibodies bound to BM

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7
Q

Goodpasture AKA

A

Antiglomerular basement membrane disease or anti-GBM disease

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8
Q

Renal characteristics associated with goodpasture

A

Involves glomeruli
Explosive acceleration of disease–>Rapidly progressive glomerulonephritis or crescentic glomerulonephritis
Urine output declines with hematuria and fluid retention with edema. Build up of urea and other wastes in blood

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9
Q

What is the most common glomerulonephritis?

A

IgA nephropathy (Berger diseasE)

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10
Q

Pathogenesis of IgA nephropathy?

A

Mucosal exposure to viral or bacterial antigens. Stimulates nephritogenic IgA dominant immune complexes within the glomeruli and mesangium which activate complement

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11
Q

IF dx for IgA nephropathy?

A

Essential for dx. Mesangial staining for IgA and C3 needed for dx. Severe–>staining of glomerular capillar wall suggests less favorable prognosis

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12
Q

EM of IgA nephropathy

A

Mesangial electron dense deposits under GBM, severe cases, deposits in capillary walls

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13
Q

Alport syndrome

A

X-linked; Abnormal Type IV collagen;

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14
Q

EM of alport syndrome

A

Most diagnostic
Irregularly thickened glomerular BM with splitting of lamina densa into interlacing string like lamina that surround electron lucent areas

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15
Q

Sx of alport

A

Hematuria, proteinuria, progressif renal failure and HTN

Hearing impariement, defect to lens

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16
Q

Thin glomerular BM disease

A

Hematuira due to thinning and rupure of the GBM
Dx: Biopsy and EM not Light micro
AD inheritance

17
Q

Type I Membranoproliferative Glomerulonephritis AKA

A

Mesangiocapillary glomerulonephritis

18
Q

Secondary causes of Type I Membranoproliferative Glomerulonephritis

A

Subacute bacterial endocarditis
Osteomylitis
Hep B virus infection
Neoplasia

19
Q

Silver stain of Type I Membranoproliferative Glomerulonephritis

A

Doubling or tram track replication of GBMs from thickened capillary walls

20
Q

AKA for Type II Membranoproliferative Glomerulonephritis

A

Dense deposit disease

21
Q

IF of Type II Membranoproliferative Glomerulonephritis

A

Linear staining of capillary walls and mesangial nodules for Complement C3 little or no staining for immunoglobulins

22
Q

Lupus nephritis

A

AI and immune complexes deposited in glomerular capillary loops–>complement–>Tissue injury

23
Q

Histo classification of Lupus nephritis- most severe

A

IV diffuse proliferative: Most serious; mesangial and subendothelial deposits; Moderate nephritis

24
Q

Class I and Class I Lupus nephritis on EM

A

Mesangial deposits

25
Q

Class V Lupus nephritis on EM

A

Several subepithelial dense deposits

26
Q

IF of Lupus nephritis

A

Subepithelial and subendothelial complexes are granular

27
Q

Lab findings of Lupus nephritis

A
Elevated BUN/Creatinine
Ua proteinuria 
Leukocytes and casts 
Autoab: AntidsDNA and Anti smith 
Serum complement decreased-->Active renal disease