Glomerular Disease 1 Flashcards

(41 cards)

1
Q

how does glomerular disease present?

A

Hematuria (quality)

Loss of GFR (temporal change)

Proteinuria (quantity)

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2
Q

factors of nephrotic syndrome

A

Proteinuria >3.5 g/day

Hypoalbuminemia

Edema

Hyperlipidemia (increased hepatic production)

Lipiduria

Hypercaogulabiltiy (loss of anticoag C and S)

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3
Q

nephrtitis

A

mild proteinuria

**Hematuria **(RBCs, RBC casts, dysmorphic RBCs)

HTN

Edema

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4
Q

causes of acute glomerulonephritis

A

IgA nephropathy

Post-infectious GN

Anti-GMB disease / good pastures

small vessel vasculitis

lupus nephritis

membranproliferative GN

(I poop good, small, little, marbels)

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5
Q

most common Gn

A

IgA nephropahty

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6
Q

most prominent feature IgA nephropathy

A

hematuria (50-60% episodic, 30% persistent, 10% acute Gn or nerphtoic syndrome)

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7
Q

presentation IgA nephropathy

A

Dysuria

Loin Pain

Hematuria

co-present w/ URI (synpharrngitic hematuria)

pos HTN

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8
Q

Histology IgA nephopathy

A

LM - messangianl hypercellularity, scelorosis+necrosis with crescents

IF: **Msangial IgA deposition **

EM- mesangional paramesangial elctron dense deposits

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9
Q

treatment IgA nephropathy

A

fish oil may slow

ACE

corticosteroids or other immunosuppresants

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10
Q

presentation Henoch-Schonlein Purpura

A

skin non blanching pupura on legs+buttucks

transient arthraligias

GI (hematochezia)

kidney - hematuria, proteinuria

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11
Q

infection presentation post infectious GN

A

7-14 days post pahryngitis, 14-28 post skin infection (esp A beta hemolytic strep)

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12
Q

clinical presentatiion Post strep GN

A

sudden onset HTN

azotemia

oliguria

edema

tea-colored urine

**Labs: **low C3 comp, ASO elevated, RBC casts in urine, proteinuria

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13
Q

histo post strep GN

A

LM - enlarged hypercell. glomeruli

diffuse mesangial+endocapilary proliferation with PMNs

crescents

**IF **granular capillary wall, mesangial IgG and C3

EM: Mesangial and large subepithelial humb-like deposits

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14
Q

causes of rapidly progressive GN

description

A

classic nephritic syndrome with rapid progression to renal failure

anti GBM / Goodpastures

ANCA asssociated GN (Pauci Immune)

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15
Q

histo rapidily progressive GN

A

crescentic

early segmental necrosis early

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16
Q

cause of Anti GBM / goodpastures

A

circulating anti GBM antibody (antigen is a3chain of type IV collagen)

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17
Q

posible presentation of Anti-GBM ./ goodpastures

A

Males>femailes

pulmonary renal syndome: hemoptysis, pulmonary infiltrates, glomerulonephritis

18
Q

diagnosis/ treatment anti-GBM / goodpastures

A

antiGBM in blood

Linear IgG and C3 on kidney biospy IF

plasmapheresis, prednisone, cytoxan

19
Q

crescenteric GN with little deposition of immune reactants

20
Q

pauci - immune GN possibly associated with

A

ANCA vasculititis

21
Q

differentiation

microscopic polyangiitis

wegner’s granulomatosis

churg straus

A

**microscopic polyangiitis: **no granulomatous inflam, no asthma

wegner’s granulomatosis: necrtizing granulomatous inflam, no asthma

**churg strauss: **necrotizing granulomatous inflam, asthma, eosinophilia

22
Q

renal biopsy wegenrs

A

cresenteric GN without immune deposits

23
Q

treatment for all causes of nephrotic syndrome

A

ACE/ARBs to lower pressure+reduce proteinuria

Statins reduce lipids

diuretics+salt restriction to improve edema

24
Q

most common cause of nephrotic syndrome in children

A

minimal change disease

25
adult associations minimal change disease
NSAIDs neoplasms esp Hodgkins Lymphoma Syphilis, HIV
26
histo Minimal change disease
LM: glmeruli intersitium and tubules normal IF negative or mesangial IgM EM: **podocyte foot process effacement (fusion)**
27
treatment minimal change disease
corticosteroids (adults take longer, more remission)
28
most common cause of nephrotic syndrome in cuacasian adults
membranous nephropathy
29
secondary causes membranous nephrpathy
infection (**HBV**) Connective tissue disease (**SLE**) Neoplasms: **carcinoma of lung, colon, stomach or breast, Non hodkin's lymphoma** Drugs
30
presentation membranous nephropathy
heavy proteinuria and nephrotic syndrome HTN and azotemia later renal vein thrombosis in 20%
31
histo membranous nephropathy
LM: **diffuse thickening of GBM, GBM spikes on silver stain** IF: granular GBM deposits of IgG EM: subepithelial depsoits
32
membranous nephropathy outcome
1/3 spontaneous remission 1/3 partial remissions + stable 1/3 slow progressive loss of renal function
33
treatment Membranous neropathy
ok prognosis : ACE or ARB poor prognosis : steroids or other immunosuprresion
34
most common casue of nephrotic syndrome in African americans
focal segmental glomerulosclerosis
35
presentation focal segmental glomerulosclerosis
HTN Hematuria end stage renal disease in 5 years primary = acute onset nephrotic syndrome secondary: slow renal insufficiency+ proteinuria
36
cauases secondary FSGS
Drugs - NSAIDs, heroin infections HIV obesity past glomerular injury loss of renal mass
37
histology focal segmental glomerular sclerosis
LM: glomerular scloeriss with capilalry colapse, hyaline and lipid deposits in bowman's capsule IF: negative or IgM and c3 in mesangium or in segmental scars EM: podocyte foot process effacemen,t segmental sclerosis
38
treatment FSGS
ACE, corticosteroids,
39
presentation membranoproliferative glomerulonephrtiis
proteinuria+hematuria HTN **low C3 complement** variable (nephrotic/asympotomatic preteinuria+hematuria/acute GN)
40
secondary causss PRGN
connective tissue disease (SLE) Cryoglobulinemia Infection: **Hep C, **Hep B, endocarditis, abscesses neoplasm
41
histo MPGN
LM: hypercellular glomeruli, endocapillary prlif, lobular apparing glomeruli IF: granular C3 depotsits EM: subendothelial deposits