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DT3-Exam 3 > Glomerular Disease--Leah** > Flashcards

Glomerular Disease--Leah** Flashcards

1
Q

Percent body mass of kidney + percent of cardiac output supplied to kidney?

A

Kidney is 0.5% body mass and receives 20% of the heart’s cardiac output… which makes sense because the kidney is responsible for filtering the blood!

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2
Q

What is the name of the kidney’s filtration unit?

What are its three layers?

A

Glomerulus: (Outer to inner)
epithelium (parietal and visceral)–>
basement membrane –>
endothelium

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3
Q

Describe the glomerular visceral epithelium:

*Also, where is the parietal epi?

A

visceral:
- composed of podocytes, which have foot processes
- “slit diaphragm” is found between each foot process

parietal:
lines bowmans CAPSULE, structural/ supportive in nature; doesn’t play a role in filtration

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4
Q

What are the three layers of the glomerular basement membrane

A

lamina rara externa
lamina densa
lamina rara interna

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5
Q

Describe the glomerular endothelium

A

highly FENESTRATED

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6
Q

What are the “support” cells for glomerular capillary tufts and basement membrane?
Why does this matter?

A

mesangial cells –> some glomerular diseases specifically target these support cells (ex: IgA nephropathy)

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7
Q

What is present in plasma that SHOULD NOT be present in glomerular filtrate? What is glomerular filtrate?

A

PROTEIN!

Glomerular filtrate is “pre-urine”, formed in the glomerulus before passage through the nephron.
Protein should be blocked by the filtration barrier and should not enter the tubule –> therefore no urinary protein

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8
Q

Nephritic vs nephrotic syndrome: what are the MAIN pathologies for these two syndromes?

What are the MAIN urinary findings for each?

A

Nephr(I)tic Syndrome:
(I)nflammatory GBM disruption–> capillary rupture–> HEMATURIA

Nephr(O) Syndrome:
P(O)docytes –> Pr(O)teinuria (3.5+g/day)

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9
Q

How much protein is seen in nephritic syndrome? Nephrotic?

A

Nephritic- 3.5 mg/day or less

NephrOtic- PrOtein!!!! MORE than 3.5 mg/day

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10
Q

Some diseases present only with nephrotic or nephritic syndromes. Others are on a spectrum and can have both symptom sets.

What is one way to remember diseases that are capable of having NephrITIC findings?

A

RAPID-M are diseases that can be nephritic
*Note, not all diseases in this mnemonic are covered by Norton, but they are in FA.

R: Rapidly progressing glomuerulonephritis
A: Alport Syndrome
P: Post Strep Glomerulonephritis (“acute proliferative”)
I: IgA nephropathy
D: Diffuse proliferative glomerulonephritis (lupus nephropathy)
M: membranoproliferative glomerulonephritis

**Note: D and M can have nephritic and/or nephrotic findings, RAPI usually stick to NEPHRITIC

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11
Q

Aside from hematuria and small amounts of protein, what might be assc with nephritic syndrome? (3)
(Urine, blood, and systemically)

A
  • red casts, oliguria
  • azotemia
  • HTN/edema, esp periorbital
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12
Q 
Acute Proliferative Glomuerulonephritis: 
Who gets it and when? 
How is it mediated? 
What are the symptoms? 
What do we do?
A
  • Within one month of GAS pharyngitis/impetigo
  • Occurs WITH OR WITHOUT ABX treatment
  • Kids ages 6-10 (mostly)
  • Immune complex mediated (Type III)
  • Self limiting; symptomatic control only
  • Worse prognosis if an adult contracts PSGN (rare)
  • Pure NEPHRITIC SYNDROME. (nephritic symptoms)
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13
Q

Post Strep GN, describe findings on:

  • LM:
  • IF:
  • EM:
A
  • LM: glom. proliferation (hypercellular- ^ neutros/monos)
  • IF: lumpy, IgG/M + C3 deposits at mesangium/GBM
  • EM: SUBEPITHELIAL HUMPS of IMMUNE COMPLEXES
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14
Q

What is Nonstreptococcal Acute Glomerulonephritis?

A

Exact same thing as PSGN but is caused by some other bacterial bacteria, virus, or parasite

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15
Q

Rapid Progressive Glomerulonephritis:

  • What is the “general” cause? Symptoms? Outcome?
  • What are the two most common histo findings assc with all three types of RPGN?
A
  • Immune mediated process; rapid = bad, TRANSPLANT!
  • Nephritic type symptoms

Histo:
-RUPTURES in the glomerular BM –> inflammatory mediators in urinary space–>

-“CRESCENTS”- BOWMANS CAPSULE-PARIETAL EPI PROLIFERATION w/ fibrin/fibrinogen and monos/MQs!!!!!!

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16
Q

Type I Rapid Progressive Glomerulonephritis is assc with what pathology/ disease?

A

Goodpastures- (hematuria and hemoptysis)

Anti-GBM Abs

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17
Q

Type II Rapid Progressive Glomerulonephritis is assc with what pathology/ diseases?

A

Immune complexes
-Idiopathic/ lupus nephritis
(PLEASE NOTE: this is NOT the most common nephropathy in lupus patients.)

  • Henoch Schoenlein Purpura
  • Severe sequelae of PSGN (RARE, see more in adults)
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18
Q

Type III Rapid Progressive Glomerulonephritis is assc with what pathology/ diseases?

A

PAUCI IMMUNE!!!!!
Idiopathic or vasculidities
-Wegners (PR3+)
-Microscopic Polyangiitis (MPO+)

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19
Q

Type I, II, III RPGN what is seen on IF

A

I: linear Ig/complement, remember this is an Ab disease!
II: granular immune complexes, this is an IC disease!
III. little/ no deposition, this is pauci-immune!!!!

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20
Q

Type I RPGN what is seen on:
LM:
IF:
EM:

A

LM: crescents
IF: linear IgG/ complement GBM deposits
EM: GBM ruptures

–Note: linear IgG looks like SMOKE.–

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21
Q

Type II RPGN what is seen on:
LM:
IF:
EM:

A

LM: crescents
IF: granular immune complexes on GBM
EM: GM ruptures AND immune complex deposits

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22
Q

Type III RPGN what is seen on:
LM:
IF:
EM:

A

LM: crescents
IF: PAUCI IMMUNE! NOTHING!
EM: GBM ruptures

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23
Q

One treatment for Type I RPGN caused by Goodpastures:?

How are all the others treated?

A

Plasmapheresis may remove the circulating anti-GBM Ab’s

*Others are treated with steroids

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24
Q

In nephrotic syndrome, aside from ^^proteinuria, what findings may be seen? (urine, blood, systemic)

A
  • ^ fat, albumin, globulins in urine (OVER 3.5 g/day protein)
  • Hyperlipidemia/ Hypoalbuminemia
  • edema
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25
Q

Membranous Nephropathy:
Who gets it?
What kind of symptom set does it have?
What is its most common cause?

A

1 NEPHROTIC syndrome in (WHITE) ADULTS

  • May be caused by lupus, malignancies, tumors, and a number of other things
  • IDIOPATHIC IMMUNE COMPLEX DEPOSITION IS THE #1 CAUSE!
26
Q

Membranous nephropathy: What is seen on:
LM:
IF:
EM:

A

LM: THICK capillaries and GBM
IF: granular, immune complexes (IgG/C3) in GBM
EM: SUBEPITHELIAL deposits = SPIKES AND DOMES (BM proliferation); effaced podocytes

27
Q

Membranous Nephropathy:
How does it present?
Whats the treatment situation?
How fatal is this? Who has better prognosis?

A

Presents with MILD proteinuria (LESS than 3.5g/day), hematuria, HTN but is STILL NEPHROTIC!!!

Treatment:

  • Steroids and immunosupressives not really effective
  • 10% die/ have renal failure in 10 years; better prog for women + patients with less proteinuria
28
Q 
Minimal Change Disease: 
Who gets this?
What causes it?
What kind of symptom set does it have? 
How do you treat it?
A
  • Kids ages 2-6 after immunization, illness
  • unkown cause, probably immuno
  • nephrotic symptoms w/ SELECTIVE ALBUMINURIA
  • responds WELL to steroids (unlike membranous nephropathy)
29
Q 
Minimal Change Disease: 
What is seen on.... 
LM:
IF: 
EM:
A

LM/IF: nothing
EM: effacement of podocytes
(hence the name “minimal change”)

30
Q 
Focal Segmental glomerulonecrosis:
Who gets this?
What kind of symptom set does it have?
How is it treated?
What is the pathogenesis?
A
  • # 1 NEPHROTIC SYNDROME in HIV, black/hispanic populations (but kids + adults can get it)
  • Nephrotic sx
  • UNRESPONSIVE to STEROIDS
  • “visceral epithelial damage” –> hyalinosis and sclerosis; genetic in some cases
31
Q

What 2 genes are assc with inherited focal segmental glomerulonecrosis

A

NPHS1-nephrin
NPHS2- podocin
*Note, genetic forms are uncommon

32
Q 
Focal segmental glomerulosclerosis:
What is seen on:
LM:
IF: 
EM:
A

LM: FOCAL, SEGMENTAL sclerosis of glomeruli–> capillary collapse/ hyalinolysis
IF: IgM/C3 in sclerotic areas +/- mesangium
EM: effacement of podocytes; epi detachment from GBM

33
Q

Outcome of focal segmental glomerulosclerosis

A
  • Bad esp in adults; can progress rapidly

- NO STEROID RESPONSE; may recur after transplant

34
Q

Causes of Type 1 and 2 Membranoproliferative glomerulonephritis?
Symptom set for this disease?

A
  • Type 1: can be idiopathic or secondary to immune disorders like HIV, Hep, SLE, schisto etc
  • Type 2: ALWAYS idiopathic
  • Can present as NEPHRITIC or NEPHROTIC

(I remember that this is the “M” in RAPID-M, as opposed to membranous, because the name is super long. Long name= complicated disease = mixed presentation)

35
Q

Type I/II membranoproliferative glomerulonephritis:

pathogenesis?

A

I: Immune complex –> classic + alternative complement
II: Alternative complement

36
Q 
Membranoproliferative glomerulonephritis type I 
What is seen on:
LM:
IF: 
EM:
A

LM: Mesangial/ Endothelial proliferation = hypercellular; TRAM TRACK splitting of GBM
IF : Granular C3, IgG, C1q, C4 (classical + alternative)
EM: subENDOthelial deposits (+/- subEPI or mesangial deposits)

37
Q 
Membranoproliferative glomerulonephritis type II 
What is seen on:
LM:
IF: 
EM:
A

LM: Mesangial/ Endothelial proliferation = hypercellular; TRAM TRACK splitting of GBM
IF: C3 deposition only (alternative complement)
EM: dense deposits in GBM = RIBBON LIKE

38
Q

What are the three “isolated glomerular abnormalities”?

A

IgA nephropathy, Alport Syndrome, Thin BM Lesion

*Note: IgA/Alport Are classified with nephritic disease in FA: R(A)P(I)D-M

39
Q

IgA nephropathy:
Cause?
If you could describe the histology for this in one word, what would it be? .

A
  • Genetic/ acquired; or follows mucosal based infection Assc with HENOCH SCHONLEIN PURPURA
  • Histo= MESANGIAL! everything happens in the mesangium.
40
Q 
IgA nepropathy:
What is seen on: 
LM:
IF: 
EM:
A

LM: mesangial + endocapillary proliferation–> widened mesangium
IF: Mesangial IgA IC deposits –> sometimes IgG/M,C3
EM: dense mesangial deposits

41
Q

What is Henoch Schonlein Purpura again?

A
  • # 1 Vasculitis in kids
  • follows URI usually
  • see purpura, arthritis, abdominal pain +/- IgA nephropathy.
42
Q

In general, What is Diffuse Proliferative Glomerulonephritis?
(Norton Doesn’t Discuss, its important. Rx question. YES IT IS SO IMPORTANT!!!)

A

-“Lupus” nephropathy
-Mixed nephritic-nephrotic (obviously, its lupus, why would it make up its mind?)
-“wire looping” on LM is pathonogmonic.
LUPus causes LOOPing.

She lists lupus as the possible cause for lots of these conditions, but on step if you see lupus, think DPGN (It’s the #1 kidney problem associated with lupus I think!)

43
Q

Alport Syndrome:

Most common genetic cause + classic triad?

A

-X linked collaged IV deficit effecting GBM
(although AD/AR forms do exist)
-“Cant see cant pee cant hear a bee!”
(neuro deficits in sight/ hearing + nephritic syndrome w/ hematuria and red cell casts)

44
Q

Quickly! Where are collagen I-IV found?

A 
"Strong, slimy, bloody, BM!"
I = bones, skin etc.
II- cartilage, vitreous
III-vascular tissue
IV- basement membranes
45
Q

Compare AD/AR forms of Alport with X linked.

Which one do you need to worry about for step?

A
  • X linked matters for step1 : causes abnormal “A5” collagen
  • AD/AR have collagen A3/4
46
Q

Alport Syndrome: EM findings

A

Early GBM thinning–> Late GBM thickening and thinning + splitting of lamina densa

47
Q

Benign Familial Hematuria:
AKA? Primary Symptom?
morphology?
Could be mistaken for?

A
  • Thin BM lesion
  • Thinning of GBM leads to asymptomatic hematuria +/- proteinuria w/ preserved renal function
  • Must distinguish from IgA or Alports.
48
Q 
Disease assc with subepithelial deposits?  (2)
subendothelial desosits (1) ? Mesangial (1)?
A

EPI: PSGN (humps); membranous (spikes/ domes)
ENDO: membranoproliferative GN type I
Mesangial: IgA nephropathy

49
Q

Three diseases that have “podocyte effacement”?

Which responds to steroids?

A
  • membranous nephropathy
  • minimal change disease
  • focal segmental glomerulonephritis

*Only minimal change will respond well to steroids

50
Q

Chronic Glomerulonephritis is the end stage for what diseases?

A

All of the really long named ones
(Rapidly Progressing, membranoproliferative, focal segmental), IgA nephropathy, and RARELY PGSN (in adults).

**Also note that it does not HAVE to be preceded by disease.

51
Q

What does chronic Glomerulonephritis look like? (3)

How does that change if it is assc with dialysis?

A
  • Shrunken kidney
  • atrophied glomeruli/ tubules
  • HTN–> hyalinized, sclerotic vasculature
    (Basically, the kidney dies)

If dialysis is assc–> ~stones, cysts, and intimal thickening (which is kind of the same as vascular sclerosis?)

52
Q

Systemic Findings Assc with Chronic Glomerulonephritis: (3)

A
  • uremic pericarditis/ gastroenteritis
  • LVH
  • HYPERparathyroid
53
Q

What is lupus nephritis?

A

Norton says: It can be anything (nephritic, nephrotic, chronic failure, HTN), probably true.

First Aid Says: Diffuse Proliferative Glomerulonephritis.
*LOOPING on light microscopy is Pathonogmonic for this.

54
Q

Who gets Henoch Schonlein Purpura?
In the Kidney, what disease does its histology match?
How do you treat it?

A
  • 3-8 year olds get this post URI, it is a form of Vasculitis.
  • # 1 vasculitis in kiddos.
  • In the kidney, this mimics IgA nephropathy (remember- that’s the one effecting the MESANGIUM); may even be same disease
  • No real treatment, just supportive. Kids generally recover but may have bouts of bloody pee for the next several years. 😕
55
Q

What’s the classic triad for Henoch Schonlein?

A

Purpuric Lesions, arthralgias, GI distress.

+ Hematuira in this case, if kidneys are effected.

56
Q

What does Henoch Schonlein look like in vessels?

A

Necrosis, IgA deposits, sub epi hemorrhage (hence Purpura)

57
Q

How common is diabetic nephropathy?
How can we prevent it?
How does it progress?

A

40% of diabetics get this! It’s super common! YOU BETTER PUT THESE GUYS ON ACEi!!!!!!!
Diabetes is the NUMBER ONE reason for dialysis!
(Dr Goebel pimped me on this once, and I knew the answer, and the resident didn’t. I wanted to squeal/ make happy sounds. I refrained though.)

Proteinuria is the first sign –> progresses to nephrotic syndrome –> leads to full blown renal failure.

58
Q

How does diabetes cause nephropathy in the first place?

A

Glycosylation (tons of glucose available) of proteins in the GBM

59
Q

What does Diabetic Nephropathy look like on Histo? (3)

What is the special body assc with this condition?

A

Glomerular hypertrophy –> increased GFR
Thick capillary BM
Sclerotic mesangial + glomerular cells.

KIMMELSTEIL-WILSON BODIES–> Thick/hyalinized glomerulus (both glomerular + mesangial cells thicken)

60
Q

In amyloidosis, where in the kidney can amyloid deposit?
What does this cause?
What kind of symptom set does it have?
REMIND ME: How does amyloid stain?

A

-It can deposit in basically any part of the kidney
(Interstitium, mesangium, glomerular caps, vessels)
-Initially presents as a NEPHROTIC syndrome –> possible DEATH by UREMIA
- *Nephrotic because it is not in the RAPID-M mnemonic!
- Neither is Diabetic nephropathy! Both are NEPHROTIC.
-STAINS WITH CONGO RED!! Can have apple green crystals on EM.

Please don’t automatically assc amyloid with Alzheimer’s. I have made this mistake twice on Rx now! Congo red should not always be a knee jerk for Alzheimer’s. It can be found in multiple myeloma and multiple other heme diseases!!!

61
Q

With what disease are nephrin and podocin assc?

A

Focal Segmental Glomerulosclerosis
(NPHS1= nephrin, NPHS2= podocin)
*Note, inherited forms of this disease are rare

DT3-Exam 3 (9 decks)

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