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Flashcards in nephritic pathology Deck (21):
1

Acute nephritic syndrome hallmarks

Increased glomerular capillary permeability (hematuria and proteinuria) and decreased glomerular filtration rate (Na and H20 retention, azotemia and hyperkalemia)

2

What is chronic renal failure

nephron loss leads to decreased GFR, uremia

3

Define focal vs diffuse

Focal affects 50%

4

Define segmental vs global

Segmental affects part of a glomerulus whereas global affects the whole glomerulus

5

What is thin basement membrane disease

AKA benign familial hematuria. Mutations in genes for collagen IV. Diagnosed based on EM

6

Alports Disease triad, cause/genetics, presentation

•Triad of nephritis, deafness, and ocular lesions. Due to X-linked mutation in alpha-5 chain of collagen IV. Cant form normal basement membranes. Diagnosed by basket-weave pattern on electron microscopy. Usually progresses to end stage renal disease

7

Types of proliferative glomerulonephritis

Endocapillary (occlusion of capillary loops), Mesangial, Epithelial – crescents (reaction to severe injury to, glomerular capillaries), Inflammatory cells

8

IgA nephropathy presentation, morphology, pathogen, therapy and prognosis

Usually asymptomatic hematuria, can be nephritic or nephrotic; often coincides with URI or GI infection, liver disease. Usually focal mesangial (can be MPGN). Mesangial IgA and complement are pathogen. Therapy is steroids and some progress to ESRD

9

Henoch-Schonlein purpura presentation and cause

Systemic IgA vasculitis due to deposition of IgA immune complexes. May involve kidneys, skin, joints, GI tract. Renal biopsy looks like IgA nephropathy. Usually occurs in kids <10 and is often after URI. Presents with purpuric rash on arms and legs

10

Post infectious glomerulonephropathy clinical, morphology

Usually poststreptococcal infections (other bacterial etiologies possible), acute nephritic syndrome. Causes a diffuse, proliferative, exudative glomerulonephropathy

11

Post-infectious GN pathology,serology, therapy and prognossi

Exogenous immune complexes result in subepithelial deposits, granular glomerular basemement membrane on IF with a starry sky appearance. Serology shows elevated anti-streptolysin O. Therapy is supportive ad 99% of children recover completely while 60% of adults recover completely

12

Crescentic glomerulonephritis cause and presentation

Crescents: histologic sign of severe acute glomerular disease. Caused by fibrinoid necrosis of capillaries. Presents as rapidly progressing glomerulonephropathy. Glomeruli usually heal with a scaar
Crescents: histologic sign of severe acute glomerular disease. Caused by fibrinoid necrosis of capillaries. Presents as rapidly progressing glomerulonephropathy. Glomeruli usually heal with a scaar

13

Which focal segmental necrotizing and cresentic glomerulonephritis have linear IF staining

Goodpastures and anti-GBM

14

Which focal segmental necrotizing and cresentic glomerulonephritis have granular IF staining

IgA, SLE, endocarditis, idiopathic

15

Which focal segmental necrotizing and cresentic glomerulonephritis have NO IF staining

Wegeners, microscopic PAN, Churg-Strauss, idiopathic

16

List serum studies for goodpastures, lupus, vasculitis and endocarditis

Goodpastures: anti-GBM Abs. Lupus: ANA, anti-dsDNA, complement depletion (C3 & C4). Vasculitis: ANCA (ex. MPO – cationic protein that can fix complement). Endocarditis: blood cultures

17

Anti-glomerular basement membrane disease cause and presentation

Caused by IgG against collagen IV in basement membrane. If reanl only, anti-GBM disease. If renal and lung, goodpastures. Presents as rapidly progressive glomerulonephritis and hemoptysis. Linear appearance on IF

18

Crescentic glomerulonephritis clinical, morphology, pathogen, therapy and prognosis

Usually RPGN with crescents on morphology. Caused by immune complexes, anti-GBM, systemic disease (pauci-immune vasculitis, SLE). Therapy is steroids, cytotoxics, plasmaphoresis and prognosis is poor.

19

Lupus nephritis cause, pathology, presentation

Caused by anti-ANA and anti-dsDNA immune complex deposition. IF shows granular immune-complex pattern with positive IgG, IgA, IgM, C1q, and C3. Presents as nephritic, nephrotic, RPGN, or mixed nephritic/nephrotic

20

WHO classification of Renal lupus

Class I: minimal changes by light microscopy. Class II: Mesangial glomerulitis (A: Normal by light microscopy. Mesangial deposits by EM and/or IF. B: mild/ moderate mesangial hypercellularity/sclerosis). Class III: Focal, segmental glomerulonephritis. Class IV: Diffuse glomerulonephritis. Class V: membranous nephropathy

21

Treatment of lupus nephritis

steroids, cytotoxics