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Flashcards in 6 Glomerular disease Deck (38):
0

3 different kinds of immune kidney disease

1) Immune complex deposition between endothelum and BM as well as deposition in BM and subepithelium.
2) Antibodies to BM or to glomerular antigens
3) Cytokines created by inflammatory cells

1

Nephrotic syndrome

*Proteinuria >3.5g/day
*Hypoalbuminemia
*Edema from loss of plasma oncotic pressure
*Hyperlipidemia

(lipiduria and hypocoaguability from C and S loss)

2

Nephritic

* Mild proteinuria
* Hematuria- RBCs, RBC casts, and dysmorphic RBCs
* HTN
* Edema

3

Acute Glomerulonephritis causes

*IgA Nephropathy
* post infectious GN
* Anti GBM disease/ Goodpasteure's
* Small vessel Vasculitis
*Lupis Nephritis
* Membranoproliferative glomerulonephritis

4

IgA Nephropathy Clinical presentation

Nephrotic and Nephritic
1) Hematuria (frequently with URI)
*50-60% episodic gross hematuria
*30% persistant microhematuria
*10% acute GN or nephrotic syndrome
2) Proteinuria
3) Dysuria and loin pain
4) HTN in advanced patients

5

IgA Nephropathy Histo

* Mesangial hypercellularity
* IF: mesangial IgA deposition
* EM: Electron dense deposits

6

IgA nephropathy course and management

*40% will develop CKD
* Fish oil may low progression
* ACEi for BP control
* Corticosteroids may be helpful for progressive disease

7

Henoch-Schoenlein Purpura Presenation

* Small vessel vasculitis
* IgA Deposition in skin and many organs
* Lower body nonblanching purpura
* Arthralgias
* ABD pain, vomiting, melena, hematochzia
* hematuria, proteinuria, Rare RF

8

Post- infectious GN

Nephritic
*HTN, azotemia, oliguria, cola/tea colored urine
*low c3
*anti streptolysin O
*RBC casts
*Mild proteinuria
*follows GAS- 7-14d post pharyngitis, 14-28 post skin infection

9

Post-infectious GN histo

*Enlarged hypercellular glomeruli
*diffuse proliferation of mesangial, endocapillary, and neutrophils
* sometimes crescenteric
* IF: granular capillary wall and IgG and C3 in mesangium
* EM: Mesangial and sub epithelial HUMP LIKE DEPOSITS

10

Post strep GN treatment and course

95% children- conservative management
*1% KF
60% of adults recover promptly

11

Rapidly progressing progressive GN Causes

Nephritic syndrome
*Crescenteric
*Rapid progression to RF

1) Anti GBM- Goodpastures
2) Immune complex GN
*Lupis
* Post- infectious
* Cryoglobulinemia
3) Anca Assocaited GN (pauci immune)

12

Rapid progressive GN Histo

Segmental necrosis early in the disease
Cellular crescent

13

Anti GBM/Goodpasteure's Signs/causes

Nephritic
*M>F
*Hemoptysis
*Pulmonary infiltrates
* GN

Caused by circulating anti GBM
* a3 chain of collagen IV

14

Goodpastures diagnosis/treatment

*anti GBM antibody test
*Linear IgG and C3 on IF
*crescenteric

Treatment
*Plasmapheresis
* prednison
*Cytoxan

15

Pauci-immune GN

Nephritic
* Idopathic, Microscopic polyangitis, Wegeners Granulomatosis, Churg-strauss syndrome

Histo
*little immune deposition on IF
* Crescenteric
* ealy segmental necrosis

16

Wegener's Granulomatosis

Nephritic
*c-ANCA pos in 80%
*UR smptoms - sinusitis, nasal lesions, hemoptysis
*purpura
*Nephritis

Biopsy-
Pauci-immune crescenteric GN

17

Nephrotic Syndrome

Primary
*Membranous nephropathy
*Focal Segmental Glomerulosclerosis
*Minimal Change Disease (80% of kiddos with nephrotic)

Secondary:
* Diabetes, SLE, Amyloidosis
* HIV, Hep B and C, Syphilis
* NSAIDs, gold, penicillamine

18

Nephrotic syndrome treatments

*ACE or ARB to reduce proteinuria
* Statin to decrease lipids
* Diuretics and salt restriction

19

Minimal change disease course and presentation

Nephrotic
*2-6 yo.
*5% ESRD progression
* spontaneous remissionscan occur
*Steroid treatment induces remission but 75% relapse
* less relapses after puberty

20

Minimal change disease causes in adults

NSAIDs
Neoplasms HODGKINS
Syphilis/HIV

21

Minimal change histo

Appears normal on LM
IF negative or IgM positive
EM: PODOCYTE FOOT PROCESS EFFACEMENT

22

Minimal change treat

Corticosteroids (may need longer treatments in adults)

23

Membranous Nephropathy

Nephrotic
*Heavy proteinuria
*later Azotemia and HTN
*Hypercoagulability and renal vein thrombosis.

*Most common caucasian adult nephrotic disease
20% cause by secondary causes
*HBV, SLE, Neoplasm- lumg, colon, stomach, breast, non hodgkins, drugs

24

Membranous nephropathy histo

LM: GBM spikes and diffuse thickening,
IF: IgG granular deposits on GBM (Granular BM staining)
EM: Subepithelial dposits

25

Membranous neuropathy course

1/3 spontaneous remission
1/3 partial stable remission
1/3 slow progression

Treat: if no poor prognositc factors
* Sometimes ACEi or ARBs
*Steroids/immunosuppressants

26

FSGS (foccal sgmental glomerulosclerosis) overview

Nephrotic (most common AA idopathic nephrosis)
Agressive:
*HTN/HEmaturia
*Renal dysfunction
* ESRD 5-20 years later

27

FSGS Types (3)

Primary (Acute onset nephrotic syndrome)
Secondary (slow increasing proteinuria and renal insufficiency)
Hereditary ( Slight diaphragm mutations)

28

FSGS causes

*HIV
*NSAIDs/Heroin
*Massive obesity
* Previous glomerular disease
*loss of functional renal mass

29

FSGS histo

LM: focal and segmental glomerular sclerosis:
*Capillary Collapse, Hyaline and lipid deposition (adhesion to bowmans capsule

IF: Negative or IgM and C3 in mesangium or scars

E: Podocyte effacement and

30

FSGS Treatment

*ACEi to decrease proteinuria
* corticosteroids may induce remission
* immunosuppresives for relapsing and Steroid refractory
* 50% ESRD at 10 yrs.

31

Mixed nephrotic nephritic

* Membranoproliferative GN
* SLE

32

MPGN (membranoproliferative GN)

Nephrotic or nephritic
*Proteinuria and Hematuria
* HTN in 33% patients
* LOW C3

33

Secondary MPGN causes

SLE
Cryoglobulinemia
HCV, HBV, endocarditis, abscesses
Neoplasm

34

MPGN histo

*LM: Hypercellular glomeruli, endocapillary proliferation, LOBULAR GLOMERULI
* IF: Granular C3 deposition
*EM: Subendothelial deposits

35

SLE

*Can cause many different renal diseases- Commonly diffuse and proliferative GN
*Lupis with HTN is frequently GN

36

SLE nephritis Histo

LM: lotts of immune cells
EM: Subendothelial deposits

37

SLE Nephritis treatment

*BP control
*Lipid control
* Extrarenal treatments
ClassIV: 25% renal failure by 5-10 yrs