Nephritic Syndrome Flashcards

1
Q

In what nephitic syndrome you can see this

A

Post infectious

Hypercellularity

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2
Q

Humps
Hypercellullar
Granular deposit of IgG and C3
Starry sky pattern

A

Post streptococcal glomerulonephritis

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3
Q

Hypercellularity and capillary thickening
Hep B and C, CLL, Indective endocarditis, SLE, Cryoglobulinemia
Double countour/Tram track appereance
IF: IgG and C3
May have dysmorphic red blood cell

Name Type I and Type II deposits

A

Membranoproliferative glomerulonephritis

Type I- Immune complexes - Subendothelial
Type II- Dense deposits disease- intramembranous deposits of ribbon like- Circulating autoantibody C3 nephritic factor (C3NeF)
IgG is absent in type II

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4
Q

Subepithelial humps

A

Post-infectious glomerulonephritis

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5
Q

HIV/ Sickle cell patient
Mutation on the gene that codes proteins- Nephrin and Podocin
Hyalinosis and sclerosis
Effacement of foot processes
Non-selective proteinuria
Poor response to corticosteroid therapy
LM: Focal tubular segment dilation filled with proteinaceous material
EM: endothelial rubuloreticular inclusion

A

Focal Segmental Glomerulosclerosis

Hematuria
Reduced GFR and hypertension
Collapse but no crescent

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6
Q

MPO- ANCA- PANCA
classical with allergies, asthma
Increase IgE

A

Eosinophilic granulomatosis with polyangiitis

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7
Q

MPO-ANCA- pANCA
Leukocytoclastic vasculitis
NO granulomas, no nasopharyngeal involvement

A

Microscopic polyangiitis

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8
Q

Protenuria after a sore throat
“Lipoid nephrosis”
Children
Trigger: Respiratory infection or routine prophylactic immunization
Defects on the anion charge barrier
Dramatic response to steroid therapy

LM: normal
EM: Effecent of foot process, no deposits
IF: No deposits

A

Minimal Change Disease

Oval Fat bodies
Maltese cross
Fatty cast
Hypoalbuminemia
Edema
Elevated Serum cholesterol and triglycerides

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9
Q

Hyperfiltration hypothesis
SGLT2 driven alterations in tubuular glomerular feedback
Direct dilation onf afferent and indirect vasoconstriction on the efferent. Bur overtime the GFR decreases.
Microalbuminuria 30to 299 albumin per gram of creatinine
AGE-RAGE signaling axis
Release of cytokines TGF beta and VEGF
Hyaline arteriolosclerosis of renal arterioles- fibrin caps adhere to the Bowman capsule

Capillary basement membrane thickening
Diffuse mesangial sclerosis
Nodular glomerulosclerosis - Kimmelstiel Wilson disease (PAS positive)

A

Diabetic Nephropathy

Metabolic syndrome

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10
Q

Hepatitis C
Palpable purpura
Weakness
Arthalgias
Mixed IgG and IgM/IgA complex deposition
Elevated Cryoprecipitate

Renal manisfestation: Type I membranoproliferative glomerulonephritis

A

Mixed Cryoglobulinemia

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11
Q

Fibrinoid necrosis
Proliferation of parietal epithelial cells derived from Bowmans capsule
Disruption of the Basement

A

Crescentic Rapidly Profressive Glomerulonephritis

Linear deposit of IgG for Goodpasture
Granular deposits for Immune complex
Minimal deposits - For ANCA they will have positive ANCA

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12
Q

Misfolded proteins deposit in the gromeruli (All pink)
Thickening of the mesangial matrix and uneven widening of the basement membrane of glomerular capillaries
Congo Red stain
Apple birefringence

A

Amyloidosis

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13
Q

Name the 4 conditions of Nephrotic syndrome

A

Minimal change disease- children

Membranous nephropathy- older adults

Focal segmental glomerulosclerosis

Membranoproliferative glomerulonephritis and dense deposits disease

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14
Q

Subepithelial deposits with spikes and Domes

A

Membranous nephropaty

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15
Q

Follows a upper respiratory infection, Group A streptococcal phrayngeal infection
Type III hypersensitivity (IgA- anti IgA immunocomplex)
Palpable purpura on buttocks and lower extremitites
Mesangial proliferation and diffuse mesangial proliferation
IgA and sometimes IgG and C3 in the mesangial region

A

Henoch Shoelein Purpura- A vasculitis

Associated with IgA nephropaty

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16
Q

NCI domain of the alpha 3 chain of Type IV collagen
Type II hypersensitivity
Necrotizing crescentic glomerulonephritis
Linear deposits of IgG
Inspiratory crackles

A

Goodpasture syndrome - Anti GBM

RBC cast, RBC dysmorphic, Hemoptysis

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17
Q

dsDNA
Injury is because of deposition of immune complexes
Type II and Type III hypersensitivity
Neuropsychiatric manifestations
Butterfly Rash
Fibrinoid Necrosis
Lbman Sacks endocarditis
Onion skin lesion

Name the Type IV and Type III

A

SLE
Dysmorphic RBC, RBC cast, low serum of complement levels, elevated anti-dsDNA

Type III- Focal proliferative lupus nephritis have crescent, increased permeability

Type IV- Diffuse proliferative lupus nephritis “wire looping” subendothelial deposits and granular deposits

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18
Q

Type I membranoproliferative glomerulonephitis

A

Mesangial Proliferative, GBM tickening or splitting with subendothelial deposits

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19
Q

Hyperfiltration hypothesis
SGLT2 driven alterations in tubuular glomerular feedback
Direct dilation onf afferent and indirect vasoconstriction on the efferent. Bur overtime the GFR decreases.
Microalbuminuria 30to 299 albumin per gram of creatinine
AGE-RAGE signaling axis
Release of cytokines TGF beta and VEGF
Hyaline arteriolosclerosis of renal arterioles- fibrin caps adhere to the Bowman capsule

Capillary basement membrane thickening
Diffuse mesangial sclerosis
Nodular glomerulosclerosis - Kimmelstiel Wilson disease (PAS positive)

A

Diabetic Nephropathy

Metabolic syndrome

20
Q

Name the 7 conditions of Nephritic syndrome

A

Post infectious and infection associated
IgA nephropathy (Berger disease)
Crescentic Rapidly progressive glomerulonephritis
Anti GM antibody mediated disease- Goodpasture
Lupus nephritis
Henoch Schonlein Purpura
ANCA associated

21
Q

Crescentic Rapidly Profressive Glomerulonephritis
Type
I
II
III

A

Type I - Anti GM antibody- goodpasture syndrome
Type II- Immune complex mediated- Lups, Post infectious, IgA nephropathy
Type III- ANCA- Granulomatosis with polyangiitis, Eosinophilic Granulomatosis with polyangiitis, Microscopic polyangitis

22
Q

Subepitehlial basement deposits
PLA2R
Humps and Spikes - thickenin of basement because od deposits
Elderly
C5b-C9
Effacement of podocytes
IF: granular deposits both IgG and complement
Renal vein thombosis high incident

A

Membranous Nephropathy

Oval fat bodies
Fatty cast

22
Q

Which category of syndrome have:
>3.5g of preteinuria/24hr
Oval Fat bodies in urine
Maletese cross
Thrombophilia
Serum albumin less than 3 mg/dl
Edema
Hyperlipidemia
Lipiduria

A

Nephrotic syndrome

23
Q

Crescentic Rapidly Profressive Glomerulonephritis

Linear deposit of IgG for Goodpasture
Granular deposits for Immune complex
Minimal deposits - For ANCA they will have positive ANCA

A

Fibrinoid necrosis
Proliferation of parietal epithelial cells derived from Bowmans capsule
Disruption of the Basement

24
X- linked trait (COL4A5)- Type 4 collagen Affect lens of eye (cataracts), sensirineural hearing loss, oliguria Basket-weave appearance of GBM
Alport syndrome Nephritic syndrome RBC cast, oliguria,hematuria, Hypertension,
25
Decrease glycosylation of O-linked glycans in the hinge Followed by respiratory infection Gets deposited in the mesangium ( mesangial inflammation and proliferation)
IgA nephropathy : Berger syndrome Dysmorphic RBC, RBC Cast, Proteinuriia, hematuria, increase IgA
26
What is nephrotic syndrome?
A kidney disorder characterized by excessive protein loss in urine.
27
Name a primary cause of nephrotic syndrome.
Minimal change disease.
28
What is focal segmental glomerulosclerosis?
A type of nephrotic syndrome that can be primary or secondary to conditions like HIV or obesity.
29
What is membranous nephropathy also known as?
Membranous glomerulonephritis.
30
List some secondary causes of membranous nephropathy.
* Drugs (NSAIDs, penicillamine, gold) * Infections (HBV, HCV, syphilis) * SLE * Solid tumors
31
What is a common complication associated with membranous nephropathy?
Increased risk of thromboembolism.
32
Which organ is most commonly involved in amyloidosis?
Kidney.
33
What conditions predispose to amyloid deposition?
* AL amyloid * AA amyloid * Prolonged dialysis
34
Describe the light microscopy findings in minimal change disease.
Normal glomeruli with possible lipid in proximal tubule cells.
35
What does segmental sclerosis and hyalinosis indicate in kidney pathology?
Focal segmental glomerulosclerosis.
36
What is observed under immunofluorescence microscopy in focal segmental glomerulosclerosis?
Often negative, but may show nonspecific focal deposits of IgM, C3, CI.
37
What does electron microscopy reveal in minimal change disease?
Effacement of podocyte foot processes.
38
What is the 'spike and dome' appearance associated with?
Subepithelial deposits in membranous nephropathy.
39
What does a Congo red stain show in amyloidosis?
Apple-green birefringence under polarized light.
40
What light chains may be positive in AL amyloidosis?
Lambda and kappa light chains.
41
What protein is associated with AA amyloidosis?
AA protein.
42
What does mesangial expansion by amyloid fibrils indicate?
Amyloidosis.
43
True or False: Nephrotic syndrome is more common in children than adults.
True.
44
Fill in the blank: Focal segmental glomerulosclerosis is more common in _______.
Black people.
46
What us aeen in light