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Renal > Chronic Glomerulonephritis, Nephrotic syndromes > Flashcards

Chronic Glomerulonephritis, Nephrotic syndromes Flashcards

1
Q

What are the 5 clinical syndromes associated with disease of the glomerulus?

A
  1. Chronic glomerulonephritis
  2. Nephrotic syndromes
  3. Acute glomerulonephritis
  4. RPGN
  5. Asymptomatic hematuria and proteinuria
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2
Q

What is the difference between nephritic salt retention and nephrotic salt retention?

A

Nephritic syndromes are associated with active inflammation in the glomerulus. This leads to PRIMARY Na retention –> volume overload, circ. congestion

Nephrotic syndromes have massive leaks of protein across the glomerulus. This decreases serum albumin declining the oncotic pressure. This to intravascular fluid to move to extravascular compartment (contracted EABV). This leads to SECONDARY Na retention. (hypertension/cirulatory congestion are less prominent, but there is edema)

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3
Q

You run lab tests and get the following urinary sediments:
RBC casts
RBC, WBC
proteinuria 2-6gms

What is the likely problem?

A

nephritic syndrome

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4
Q

You run lab tests and get the following urinary sediments:

Oval fat bodies
Heavy proteinuria
Fatty casts
Free fat droplets

What is the likely problem?

A

Nephrotic syndrome

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5
Q

What condition is associated with:

secondary Na retention
low urine Na
edema
SLIGHTLY reduced GFR

A

Nephrotic

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6
Q

What condition is associated with

primary Na retention 
low urine Na
hypertension 
edema
circulatory congestion 
severely reduced GFR
A

nephritic syndrome

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7
Q

Chronic glomerulonephritis is a form of chronic kidney disease that is characterized by irreversible and progressive __________ and ____________ necrosis.
What does this necrosis lead to?
What is the treatment?

A

Glomerular AND tubulointerstitial necrosis.

This decreases GFR leading to retention of uremic toxins –>CKD–>ESRD–>cardiovasular disease.

The pathological changes are irreversible, so the patient is treated with blood pressure control

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8
Q

Describe the kidney gross and microscopic changes associated with chronic glomerulonephritis.

A

Grossly, the kidneys are much smaller.
Microscopically you note fibrosis and glomerulosclerosis.

Biopsy cannot usually distinguish the primary disease, because all the glomerular diseases progress to this fibrotic,sclerotic state.

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9
Q

What are the 4 main things that determine nephrotic syndrome?
What 2 major sequelae occur as a result of nephrotic syndromes?

A
  1. proteinuria (>3.5)
  2. edema
  3. hypoalbuminemia
  4. hyperlipidemia

Sequelae:

  1. hypercoagulability (anti-coag are filtered out)
  2. predisposition to infection by encapsulated G+ (loss of immunoglobin)
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10
Q

What is the primary cause of MGN?

What are the secondary causes?

A

Primary:
- autoimmune with antibody to M-type PLA2 receptor in podocytes

Secondary:

  • HepB
  • SLE, RA
  • gold, captopril
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11
Q

How does acute glomerulonephritis differ from RPGN?

How are they similar?

A

Acute - usually associated with a preceding infection (IgA nephropathy, post strep) and the GFR is relatively stable. It will rapidly resolve.

RPGN has a rapidly falling GFR. (>2mg/dl rise in Cr over 3 months). It is not temporally associated with infection and tends to not rapidly resolve.

They both have urine sediment with RBC, WBC and RBC cast.
They both are associated with hypertension

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12
Q

What specific feature characterizes RPGN from acute glomerulonephritis?

A

There is a rapid loss of renal function

Cr rises by >2mg/dl over 3 months

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13
Q

What are the 4 primary nephrotic syndromes?

What are examples of secondary/systemic?

A

Primary:

  1. MCD
  2. FSGS
  3. MGN
  4. MPGN

Secondary:

  1. SLE
  2. Diabetic nephropathy
  3. Amyloidosis
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14
Q

What is the normal urinary P/Cr ratio?

How is this measured?

A

0.15 which reflects 150mg/day loss of protein.
A standard urine dipstick is used as a screen for proteinuria (limitation is that it only records - so you need to do an SSA for + proteins)

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15
Q

What is the most common idiopathic nephrotic disease in children?
What does this disease look like on LM, EM, IF?

A

MCD

LM- normal or slight mesangial proliferation
EM- fusion of the podocytes
IF- no immune complex deposition

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16
Q

What are the 2 most important secondary causes of MCD?

How do you treat each situation?

A
  1. Hodgkins lymphoma- treat the cancer

2. NSAIDs, ampicillin, rifampin, interferon- stop drug

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17
Q

Who is most frequently affected by FSGS? What are the characteristics on LM, EM, IF?

A

AA adult males

LM- some but not all glomeruli are involved. Each glomeruli that is involved have segmental areas of sclerosis (hyaline deposits, closing off capillary lumens) and mesangial hypercellularity

IF- no immune deposits (some nonspecific IgM and complement trapping in sclerotic tissue

EM- diffuse fusion of the epithelia foot processes

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18
Q

How is the treatment of MCD and FSGS different?

A

MCD can be treated with steroids while FSGS cannot

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19
Q

Why does FSGS sometimes lead to sampling error on renal biopsy?

A

the disease is focal in nature so not all glomeruli are involved

20
Q

What is thought to be the cause of FSGS?

A
  • injury to the visceral epithelial cell or podocyte

- genes for podocin nephrin

21
Q

What is the most common potential cause of secondary focal glomerulosclerosis?

A

adaptive response to nephron loss from CKD, reflux neropathy, ischemia, reduction in renal mass
with compensatory hypertrophy and intraglomerular hypertension to maintain GFR

22
Q

What causes secondary segmental areas of glomerulosclerosis?

A

Intraglomerular hypertension from primary renal vasodilation due to:

  1. diabetes
  2. sickle cell anemia
23
Q

What determines the prognosis of FSGS?

What is treatment?

A

The amount of proteinuria.
>10 is associated with poor prognosis and can lead to ESRD w/in 5 years.

Treat with steroids for 6months, cyc A, cytotoxic agents
If these don’t work–> conservative management

24
Q

What differentiates the collapsing variant of FSGS from the non-collapsing?
Which is more severe?
Who is at a higher risk for collapsing FSGS?

A

In collapsing, there is collapse and sclerosis of the entire glomerular tuft rather than segmental injury.

Collapsing is more severe and people with HIV and black men are at higher risk for this variant.

25
Q

What is HIVAN? Who is usually affected?

Patients with this have evidence of ___________ of the _____________ in the kidney.

A

It is HIV-associated nephropathy.
It typically affects black patients with HIV.

Patients have evidence of direct viral infection of the glomerular visceral epithelial cells–> nephrotic syndrome, kidney insufficiency, ESRD.

They do NOT have hypertension or edema.

26
Q

What does a sonography of the kidney in someone with HIVAN show?
What does a biopsy show?
What is seen on EM?

A

The kidneys will be enlarged and highly echogenic.

The biopsy can show segmental OR collapsing glomerulosclerosis with tubular cystic lesions (making the kidney larger).

EM shows tubuloreticular bodies

27
Q

Describe the most common secondary causes of MGN.

Who is most frequently affected by primary membranous glomerulonephritis?

A

Primary- white adults older than 60 years of age

Secondary MGN (20% of cases)

  1. Lupus
  2. Hep B
  3. gold, penicillamine
  4. solid tumors (non-Hodgkins)
28
Q

What is seen on LM, EM, and IF for MGN?

A

LM- thickened GBM with little or no cell proliferation or infiltration

EM- electron dense deposits in the subepithelial space of the basement membrane

IF- Ig, C3 to the subepithelial deposits – granular/lumpy-bumpy

29
Q

How is MGN treated?

A

steroids, cyA and cytotoxic agents

30
Q

What are the other names for MPGN?

A

mesangiocapillary or lobular glomerulonephritis.

31
Q

When does the idiopathic form of MPGN usually occur?

What are the main causes for secondary MPGN?

A

Idiopathic occurs in people 8-30

Secondary:
Lupus, Sjogrens, Hep C, infective endocarditis

32
Q

What is seen on LM, EM and IF for MPGN?

A

LM- thickening of the GBM due to immune complex deposition and to the interposition of mesangial cell cytoplasm between the GBM and endothelial cells (TRAM TRACKING) and hypercellularity leading to lobular appearance

33
Q

What are the 3 types of MPGN?

A
  1. Type 1- immune deposits subendothelial and in the mesangium (evaluate for 2ndary)
  2. Dense deposit disease- dense ribbon-like deposits along the basement membranes of glomeruli, bowman’s capsule and tubules. (C3 nephritic factor +)
  3. Type 3- similar to 1 except the subendothelial deposits are prominent and cause GBM disruption with lucent areas
34
Q

Hypocomplementemia is a characteristic of all 3 MPGN. Which pathways are used in each type?

A
  1. classic - initiated by immune complexes
  2. aleternate pathway- increased catabolism of C3 by IgG C3 nephritic factor
  3. classic
35
Q

How do you treat MPGN?

A
  1. steroids

2. anti-platelets

36
Q

What glomerulous disease is Hep C most frequently associated with?
What is the usual outcome and what is the treatment?

A

Hep C is associated with MPGN most frequently. with or w/o cryoglobulinemia.
Hypertension and edema are common with nephrotic range proteinuria and mild nephritic sediment.
RF+, C3. C4

Treatment is IFNa, ribavirin as antiviral in patients with MPGN, but they dont work for advanced kidney failure

37
Q

What glomerular disease is most associated with Hep B?

A

MGN and nephrotic syndrome

38
Q

If there is suspicion of systemic amyloidosis, what should be biopsied?
How do they stain?

A
  1. abdominal fat
  2. rectal/duodenal mucousa
  3. kidney

They stain positive for Congo Red- apple green birefringence

39
Q

What are the 3 main types of amyloidosis?

How are they treated?

A
  1. AL - most common type and is associated with the deposit of Ig light chain (lambda usually) or a fragment. Monoclonal Ab in serum, blood or tissue (as detected by protein electrophoresis) differentiates this strain from the other.

AL is treated with chemo (melphalan and peripheral stem cell transplant)

  1. AA - deposition of amyloid A protein that is a fragment of serum amyloid A (acute phase reactant of the liver). It develops secondary to chronic inflammatory states (ulcers, RA, osteomyelitis) and injection drug use

AA is treated by attacking the underlying cause and colchicine for familial

  1. AF - familial AD disorder caused by abnormalities in transthyretin
40
Q

What 4 things constitute the clinical syndrome of diabetic nephropathy?

How long does it take to progress to renal failure?

What is the risk for IDDM vs NIDDM?

A
  1. long standing diabetes mellitus
  2. persistent albuminuria
  3. hypertension
  4. declining GFR

Progresses to renal failure in 5-10 years

IDDM- 45% progress
NIDDM - 20% progress (but there are more people with type two so its a higher incidence overall)

41
Q

What are the 4 stages of diabetic nephropathy?

A
  1. renal hypertrophy and hyperfunction
  2. clinically silent renal disease
  3. incipient nephropathy
  4. Overt diabetic nephropathy
42
Q

Describe what occurs in Stage 1 of diabetic nephropathy.

A

Kidney size and GFR are increased.

Glomeruli and tubules are enlarged and the capillary and mesangial surface areas are increased.

43
Q

Describe stage 2 of diabetic nephropathy.

A

Two to 3 years after diagnosis, GFR remains increased and albuminuria is absent.

With marked hyperglycemia or ketosis after exercise or with fever, urinary protein increases transiently.

GBM thickens and mesangium expands.

44
Q

Describe stage 3 of diabetic nephropathy.

What is treatment at this stage?

A

sustained microalbuminuria after 10-15 years of diabetes (>30 in the urine)

Total urine protein is around 150, albumin is less than 30 normally.
Microalbuminuria- the dipstick is negative

Treat with ACEI/ARB to slow progression

45
Q

Describe stage 4 diabetic nephropathy.

A
  1. clinically detectable proteinuria >500mg/day
  2. hypertension
  3. decreased GFR
46
Q

What is the pathophysiology behind the progression of diabetic nephropathy?

A

Reduced renal mass–> increased GFR in the remaining nephrons
(decreased aff and eff resistance but more in aff so the Pgc increases)
Eventually these overworking nephrons –> proteinuria–>glom sclerosis–> azotemia

Renal (11 decks)

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