308 - Glomerular Diseases (nephrotic) Flashcards

1
Q

MCD= ___

A

minimal change disease

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2
Q

MCD is usually in children (___%), and sometimes in adults (__%)

A

70-90

10-15

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3
Q

MCD is usually ____ but can be ___ to Hodgkin’s lymphoma, allergy, NSAID… The pathophysiology has to do with ___ influencing the ___ barrier

A

primary
secondary
cytokines
glomerular

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4
Q

MCD common clinical presentation include: acute ___, nephrotic syndrome ( with ___ deposition), proteinuria (>__g/24hr), and ___.

A

edema
acellular
10 g/24hr
hypoalbuminemia

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5
Q

Less common clinical presentation of MCD include: (5)

A
HTN (more in adults)
microscopic hematuria
allergic symptoms 
renal dysfunction
IS nephritis
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6
Q

Children with MCD usually have selective ___, mostly ___.

A

proteinuria

albumin

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7
Q

Diagnosed MCD will require ___ if the patient does not respond to ____

A

biopsy

steroids

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8
Q

Treatment for MCD includes- 1st line ____, 2nd ____

A

prednisone

cyclophosphamide/chlorambucil

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9
Q

In MCD primary responders are patients who undergo full remission (___ mg/24hr) after a course of prednisone.

A

0.2

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10
Q

In MCD steroid dependent patients are those with ___ during the ___ period from prednisone

A

relapses

tapering

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11
Q

Frequent relapsers MCD patients are those who have had at least ___ relapses in __ months

A

2

6

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12
Q

Steroid resistant MCD patients are those who do not respond to steroid treatment. Some of those are diagnosed with ___ in follow up biopsies

A

FSGS (Focal segmental glomerulosclerosis)

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13
Q

90-95% of children with MCD go through ___ remission after ___ weeks of steroid treatment

A

full

8

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14
Q

80-85% of ADULTS with MCD go through ___ remission after ___ weeks of steroid treatment

A

full

20-24

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15
Q

FSGS is defined by ____ scarring that does not involve the entire ___, mostly in the ____ junction.

A

segmental
glomeruli
corticomedullary

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16
Q

When performing FSGS biopsy which is not deep enough, it may not include all of the pathological findings, leading to a false diagnosis of ___

A

MCD

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17
Q

FSGS may be secondary to ___, ___, ___, ___ (4)

A

HIV
HBV
SCD
reflux nephropathy

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18
Q

The clinical presentation of FSGS may include: (3)

A

proteinuria
hematuria
HTN

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19
Q

Treating FSGS include ____ inhibitors, and when patients are not in the nephrotic range- also ___

A

RAAS

steroids

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20
Q

In secondary FSGS treatment is firstly directed for the ___ disease + ____. ____ should not be used

A

primary
proteinuria
steroids

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21
Q

Negative prognostic signs in FSGS involve: (3)

A

nephrotic range proteinuria (>3.5 g/24 hours)
Afro-American
RF

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22
Q

MGN=___

A

membranous glomerulonephritis

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23
Q

What is the most common cause for nephrotic syndrome in the adult?

A

MGN- 30%

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24
Q

MGN is more common in ___

A

men

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25
Q

25-30% of MGN cases are secondary to: (3)

A

malignancy (lung/breast/colon)
infection (HBV/malaria/schistosome)
rheumatologic (SLE/RA)

26
Q

MGN biopsy will show uniform ___ of the GBM. We will also find diffuse granular depositions of ___ and ___

A

thickening
C3
IgG

27
Q

The mechanism of primary MGN is probably due to the formation of ___ complexes in situ in reaction to ___ on the ___

A

immune
antigens
podocytes

28
Q

Clinical presentation of MGN includes: (4)

A

nephrotic syndrome
nonselective proteinuria
microscopic hematuria
high frequency of thromboembolic complications

29
Q

It might be beneficial to treat MGN patients with prophylactic ___ treatment due higher risk of ___ events. Remember they must be with prolonged ___ and no risk for ___

A

anticoagulant
thromboembolic
proteinuria
bleeding

30
Q

Treating MGN is directed to solve: (3)

A

Edema
dyslipidemia
HTN

31
Q

Treating MGN includes the following drugs: (3)

A

RAAS inhibitors
Immunosuppressive treatment
(steroids/cyclophosphamide/chlorambucil)
prophylactic anticoagulant treatment

32
Q

In MGN __ of the patients will go through spontaneous remission, ___ will suffer from relapses of ___ with no renal dysfunction, ___ will progress to ___ or ___ due to complications

A
1/3
1/3
nephrotic syndrome
1/3
RF
death
33
Q

Negative prognostic factors in MGN include (4)

A

men
old age
HTN
persistence proteinuria

34
Q

The main reason for diabetic nephropathy is ___ (45%), followed by ___(40%),

A

chronic renal failure

diabetes

35
Q

Risk factors for diabetic nephropathy include: (5)

A
hyperglycemia
HTN
dyslipidemia
smoking 
family history
36
Q

The pathophysiology of diabetic nephropathy involves the loss of the ___ of the interglomerular ___, an increased production of ___ and glomerulosclerosis

A

negative charge
GBM
matrix

37
Q

In diabetic nephropathy immunofluorescences there is a non specific deposition of ___ and ___ with no sediments in the EM + vascular changes

A

IgG

complement

38
Q

How long until pathological signs appear in diabetic nephropathy?

A

1-2 years

39
Q

Clinical presentation of diabetic nephropathy include: (3)

A

microalbuminuria (30-300 mg/24hr) < 5-10 years
albuminuria (>300 mg/24hr) > 5-10 years
retinopathy (Kimmelstiel - Wilson nodules)

40
Q

Diagnosis of diabetic nephropathy is mostly based on the following: (3)

A

normal-enlarged kidneys
diabetic retinopathy
lack of clinical/serologic signs for a different diagnosis

41
Q

Treatment for diabetic nephropathy includes- monitoring ___ levels, controlling ___ (usually > 3 drugs), ___ inhibitors. DB1 will be initially treated with ___, while DB2 with ___ or ___

A
glucose
HTN
RAAS
ACEi
ACEi/ARB
42
Q

LCDD=___

A

light chain deposition disease

43
Q

In LCDD there is an increased secretion of ___ from ___ cells that can lead to deposition in the ___/___ sites.

A

light chains
plasma cells
tubular
glomerular

44
Q

LCDD damages the kidney with cast ____- RF without substantial ___, secondary ___.

A

nephropathy
proteinuria
amyloidosis

45
Q

LCDD can also lead to ___ syndrome with ___ (__% of cases will advance to ___)

A

nephrotic
RF
70
dialysis

46
Q

We can diagnose LCDD with either ___ or ___

A

IF- light chain Ab deposition

EM- granular deposition

47
Q

Treatment for LCDD includes treating the ___ disease, and if possible- autologous ____ transplantation

A

primary

BM

48
Q

Renal amyloidosis can be __ or ___.

A

primary- AL

secondary- AA

49
Q

Primary renal amyloidosis will present with ___ deposition (75% ___ ). In 10% __ will also be present with lytic bone fractures and BM infiltration (>__ plasma cells). 20% will continue to ___.

A
light chains
lambda
MM
30%
dialysis
50
Q

Secondary renal amyloidosis common disease include: (5). It is not uncommon to see nephrotic syndrome in theses patients. 50% will reach dialysis

A
RA (40%)
psoriasis
SLE
FMF
TB
51
Q

In both forms of renal amyloidosis we will have ___, severe___, renal vein ___, heart with reactive ____, PNS with ___ syndrome, and macroglossia.

A
hepatomegaly
proteinuria
thrombosis
cardiomyopathy
carpal tunnel
52
Q

We can diagnose renal amyloidosis with ___.

A

biopsy

53
Q

Treatment for renal amyloidosis includes- primary: ___+___, secondary: treating the ___ disease

A

melphalan
autologous BM transplantation
primary

54
Q

Pulmonary renal syndrome is mainly caused by: (5)

A
Goodpasture's syndrome
Wegner's
microscopic polyangiitis
Churg Strauss
HSP
55
Q

Treatment for pulmonary renal syndrome includes: empiric ___ + ___ - before lab results are back.

A

plasmapheresis

methyl prednisone

56
Q

Basement membrane syndrome has to do with collagen type ___, which is found in different tissues such as: (5). Damage to the GBM leads to medium proteinuria, hematuria, and progressive RF

A
IV
GBM
lungs
testis
cochlea
eyes
57
Q

Remember anti GBM disease: we will find Ab against ____ of collagen __. We might see pulmonary renal syndrome (___) together with RPGN

A

Alpha 3 NC1
IV
Goodpasture’s

58
Q

Name 4 basement membrane syndrome diseases:

A

Anti GBM disease
Alport’s syndrome (X-linked)
thin membrane disease
Nail patella syndrome

59
Q

Glomerular vascular syndrome involves ___ damage to the capillaries of the ___. Most of the processes are part of a systemic damage.

A

vascular

glomeruli

60
Q

Name 5 glomerular vascular syndrome disease- (5)

A
atherosclerosis nephropathy
hypertensive nephropathy
cholesterol emboli
sickle cell disease 
Thrombotic microangiopathies (HUS/TTP)