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Medicine > Glomerular Ds > Flashcards

Glomerular Ds Flashcards

1
Q

Absolute indication for hemodialysis

Other indication

A

Uremia

Others ecg change metabolic acidosis fluid overload unresponsive to med mgt

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2
Q

Clinical features of rpgn

A

Clinical features of rpgn
Progressive facial puffiness pedal edema high colored urine that progress to oliguria htn
Bp 150/100

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3
Q

Biopsy finding of rpgn

A

Crescent
Collapse of glomeruli
Parietal epithelial proliferation along with fibrin platelet
No of crescent more than size of crescent

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4
Q

Classification of rpgn is done on basis of

A

Immunofluorscene

Type 1to5

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5
Q

Most common rogn overall

A

Type 3 >2 >1

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6
Q

Most common rpgn in 1-20 yrs age grp

A

Type 2

Immune complex deposit

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7
Q

Good pasture syndrome is type of

A

Type 1 rpgn Linear igG +c3 deposit along capillary wall

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8
Q

SLE MPGN ADULT HSP ADULT PIGN are type of

A

Type 2 RPGN immune complex deposit

IgG IgA or full house

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9
Q

Type 3 ie pauci immune is found in

A

Anca vasculitis

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10
Q

Good pasture syndrome consist of

A

Rpgn

Diffuse alveolar hemorrhage

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11
Q

What is good pasture disease

A

Rpgn
Dah
Ab against NC1 domain of alpha 3 chain of type 4 collagen

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12
Q

Only glomerular disease which has smoking as risk factor

A

RPGN- anti GBM disease

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13
Q

Confirmation test for dah (rpgn)

A

Bal sputum :hemosiderin laden macrophage
Pft increased diffusing capacity of lungs for carbon monoxide
Bronchoscopy blood in air spaces

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14
Q

Most sensitive test for diffuse alveolar hemorrhage

A

Pft increased dlco

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15
Q

Most specific test for diffuse alveolar hemorrhage

A

Bal sputum

Hemosiderin laden macrophage

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16
Q

Treatment for good pasture disease

A

Plasma exchange

Steroids and cyclophosphamide for 3months

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17
Q

Anti gbm disease consists of

A

Rpgn
DAH
Anti gbm antibody

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18
Q

Type 4 rpgn i e double positive means

A

Type 1 with anti gbm and anca +

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19
Q

How to detect inheritance of alport syndrome from skin IF

A

If skin IF Abnormal - defect in alpha 5 i e x linked (80%)

If skin IF normal -defect in alpha 3&4 ie autosomal recessive or dominant

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20
Q

Pathogenesis of alport

A

Type 4 collagen alpha 1 23 class switch to

Alpha 345 - in glomerlus cochlea ocular bm

Alpha 556 epidermal bm

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21
Q

Amyloid deposit in amyloid kidney is most likely to be

A

Lambda > kappa

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22
Q

Staining characteristics to comfirm amyloid deposit

A

Extracellular hyaline amorphous nodule
Weakly pas positive
Congo red positive
Apple green birefringence on polarised microscopy

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23
Q

Polyclonal nodules can be found in

A

MPGN

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24
Q

Organized mono clonal ig deposit( lambda)

Suspect?

A

Amyloidosis

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25
Q

Secondary amyloidosis clinical feature are

A 
Nephrotic syndrome and massive proteinuria 
Autonomic neuropathy
Hepatomegaly 
Peripheral neuropathy 
Macroglossia
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26
Q

Prognosis of X linked inheritance
Autosomal recessive
Autosomal dominant

A

X linked in male progresses to esrd
AR severe esrd in both sexes
AD mild ds in both sexes

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27
Q

Manifestation of alport at the age of 5-10 yrs

A

Proteinuria htn

Start on ace

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28
Q

Manifestation of alport at the age of 5yrs and

At 10 yrs

A

Microscopic hematuria

Sr Creatinine increased

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29
Q

High or Low frequency sn hearing loss occurs at what age in alport

A

15 yrs

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30
Q

What are opthalmic manifestation of alport and at what age they appear

A

Most common dot and fleck retinopathy
Pathognomic anterior lenticonus
At the age of 20 yrs

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31
Q

Can ophthalmoscope be used to find opthalmic manifestation of alport syndrome

A

Oil drop appearance on fundoscopy

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32
Q

Thin gbm disease

Characteristics

A

Uniform thinning of GBM
No risk of Ckd
Microhematuria
No extrarenal feature

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33
Q

Basket weaven appearance
Alternating thickening and thinning of gbm
Is seen in

A

Alports syndrome

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34
Q

Prognosis after transplant in a pt of alports

A

Zero percent post transplant recurrence

5% post transplant good pasture disease in graft

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35
Q

Most common primary glomerulonephritis

A

IgA nephropathy

Aka bergers disease henoch scholein nephritis

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36
Q

Innocent bystander theory is wrt which disease

A

IgA nephropathy

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37
Q

Pathogenesis of IgA nephropathy

A 
Defective galactosylation of polymeroc IgA1 produced by malt 
Not cleared by liver
Antiglycan ab 
Immune complex
Deposit in mesangium
Kidney is innocent bystander
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38
Q

Other causes where increased polymeric IgA mucosal production leads to IGA nephropathy

A

Celiac disease
Whipples
IBS (UC>CD)

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39
Q

Other causes where defective uptake by liver lead to IgA nephropathy

A

Cirrhosis
Alcohol
NASH

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40
Q

Most common glomerular ds acc with hep B

A

Membranous nephropathy

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41
Q

1/3rd rule. Of Iga nephropathy

A

One third spontaneously resolve
“ Stable course with maintained gfr
“ CKD even with t/t

42
Q

MESTC Score is seen in which glomerular ds

A

IgA nephropathy

Mesangial hypercellularity
Endocapillary hypercellularity
Segmental sclerosis
Tubular atrophy
Crescent formation
43
Q

Can IgA nephropathy present as nephrotic syndrome or ckd

A

Less than 5% present as Nephrotic Syndrome (MCD)

Less than 5% as CKD (B/L small kidney)

44
Q

Prognostic factor of IgA nephropathy

Do serum IgA level and complement levels have no role in prognosis.?

A

Any deposit other than IgA
IgA deposition in capillary wall
Endocapillary proliferation

No, no role in diagnosis/prognosis

45
Q

Crescent formation in IgA nephropathy present as?

A

Less than 1% pt present as RPGN TYPE2

Adult Hsp

46
Q

Any sign which is responsible for good prognosis in IgA nephropathy

A

Macrohematuria

47
Q

Treatment of IgA nephropathy with respect to different presentation

A

ACEI/ARB
PROTEINURIA<500 mg
Limit salt intake
Steroids-

48
Q

Acc to clinical presentation steroid intake in pt differs
T/T in nephrotic syndrome
RPGN
Proteinuria more than 1g/day and pt on conservative therapy

A

A -treat like MCD
B- Steroid+cyclophosphamide
C- Steroid

49
Q

Causative agent of psgn in childhood and types

A

Group A Beta hemolytic strep
Type 1 3 4 12 mainly
Type 49 mainly

50
Q

Incidence of psgn is common in

A

Immunocompetent children boyrs

2-7 yrs of age

51
Q

Urinalysis of psgn will show

A

WBC casts

52
Q

Detection of toxin in psgn

Name

A

Streptococcal pyogenic exotoxin B
AntiDNase B titre
Nephritis ass plasminogen receptor (NAPL2R)

53
Q

Glomerulonephritis ass with MRSA seen in immunocompromised / diabetic foot, cellulitus pt

A

PIGN -Post infectious
Or
IRGN-Infection related GN

54
Q

In children presentation of PSGN is mostly

Treatment?

A

Acute nephritic syndrome
Benzathine penicillin 12 lakh/units IM
Steroid not indicated

55
Q

Importance of C3 levels in psgn in children

A

As psgn activate alternate complement pathway C3 levels are high
But after treatment follow up after 8 weeks C3 levels if remain high that means diagnosis was wrong
And biopsy is indicated

56
Q

In adults PIGN presents as

What is treatment and prognosis

A

Rapidly progressive renal failure
Treatment dialysis
Prognosis poor as mrsa but vancomycin cannot be given nephrotoxic and steroids or immunosuppressent also cannot be used

57
Q

Characteristics LM finding of PSGN

A

DPGN
endocapillary hypercellularity mesangial hypercellularity with neutrophil infiltration
In children DPGN
In adults DPGN +crescent

58
Q

Electron microscopic finding of psgn

A

Sub Epithelial camel hump deposit

Lumpy bumpy deposit

59
Q

Mesangiocapillary glomerulonephritis is other name for

A

MPGN

60
Q

What is podocytopathy

A

Podocyte injury resulting in proteinuria

Seen in MCD FSGS MN

61
Q

Lipoid nephrosis is other name for

A

Minimal change disease

62
Q

Primary causes of MPGN

A

None it is always secondary

63
Q

Glomerular ds with extremely high chance for recurrence post transplant

A

Almost 100% in type 2 MPGN

64
Q

Types of MPGN

A

Type 1 classical MPGN

TYPE 2 C3 GN

65
Q

Most important causes of type 1 MPGN

A

Infection- HCV, Leprosy, P. Malariae, IE

Malignancies monoclonal Immunoglobulin (plasma cell dyscrasia)

Autoimmune -cryoglobulinemia, sle3&4 , scleroderma, sjogrens syndrome

66
Q

Complement levels in TYPE 1&2 MPGN

A

Type 1 C3 &4 levels low– classical pathway

Type 2 C3 low C4 normal – alternate pathway

67
Q

Type 2 C3 MPGN Characteristic

A

Partial lipodystrophy of face
Drusen on retina
Aka dense deposit disease intramembranous deposit

68
Q

Most important manifestation of scleroderma in kidney

A

Small vessel ds(TMA)

69
Q

Most important manifestation of sjogrens in kidney

A

RTA type 1

70
Q

Light microscopy finding of MPGN

A

Mesangial Hypercellularity> endocapillary Hypercellularity
Thickening of capillary wall
Lobular capillary tuft
Uniform small nodules

71
Q

Double contour/Tram track appearance is seen in

A

Type 1MPGN

Subendothelial deposit

72
Q

Hyaline thrombi in MPGN is specific to which secondary cause

A

Cryoglobulinemia

73
Q

Only glomerular ds which can present as nephrotic and nephritic syndrome

A

MPGN

35% each

74
Q

IgG deposit +C3 in Mesangiocapillary wall can be seen in

A

mpgn

75
Q

MCD is seen most commonly in

A

Boys 2-7 yrs

90% of nephrotic syndrome in children are MCD

76
Q

3yr old boy with proteinuria no hematuria or htn or raised creat in serum
MC diagnosis

A

MCD

77
Q

Drugs responsible for MCD

A

NSAIDs

Interferon alpha

78
Q

Gold can cause which renal disorder

A

Membranous nephropathy

79
Q

Most common malignancy ass c mcd

A

Hodgkin’s lymphoma

80
Q

Why is it called MCD

A

Because LM and IF show no change ie normal

81
Q

Which type of MCD can show some changes in LM

A

IgM nephropathy can cause mild mesangial expansion and it can progresa to ckd

82
Q

EM finding in MCD

Why MCD never progress to CKD

A

Effacement of foot process of podocyte

Because no of podocyte do not decrease in MCD

83
Q

Podocyte injury in MCD can be due to

A

Increased CD80 expression in podocyte

Increase angiopoietin like 4 expression

84
Q

Specific Mgt of MCD

A

Oral prednisolone in children and adults
2mg/kg/day children
1mg/kg/day adula
Full dose in morning for 6 wks then taper for another 6 wks
Total duration 6wks
Growth monitoring and urine monitoring

85
Q

When do we say child with minimal change disease has gone into remission

A

Urine albumin is nil for 3 consecutive days

86
Q

10% children are steroid resistant

How to define it

A

Proteinuria persisiting despite full dose of steroids fo 4 wks in child and 4 month in adult

87
Q

Treatment for steroid resistant mcd

A

Calcineurin inhibitors
Tacrolimus or cyclosporin
Leavmisole

88
Q

Out of 90% responding 2/3 rd relapse -

What is relapse in mcd

A

Proteinuria reappearing after mini 4 wks of remission

89
Q

What can be the cause of relapse in minimal change disease

A

Frequent relapse -more than 2 relapse in 6 months

Steroid dependant nephrotic syndrome

90
Q

How to treat relapse in minimal change disease

A

Steroid then urine albumin become nil continue steroid for 2 more days
And start tapering

91
Q

DOC in frequent relapse in minimal change disease

A

Cyclophosphamide 2mg/kg for 12 wks

92
Q

Define steroid dependant nephrotic syndrome
Treatment
And last choice of drug

A

2 or more episode of proteinuria within 14 days of stopping steroid or while tapering

T/T calcineurin inhibitors
Last choice of drug rituximab

93
Q

Prognosis of fsgs

A

2/3rd pt progress to ckd even after treatment

94
Q

Patho of fsgs

A

Decrease in podocyte
Synechiae formation
Loss of bowman space
Sclerosis

95
Q

Types of FSGS with cause

A

Type 1 primary
Soluble urolinase plasminogen activator receptor (SUPAR) elevated

Type 2 Secondary
Drugs IFNalpha, pamidronate, sirolimus, heroin
Infection parvovirus hiv cmv ebv
Genetic

96
Q

Characteristics of secondary FSGS

A

No nephrotic syndrome
Nephrotic range proteinuria and systemic htn
LM fags
EM podocyte effacement<50%

97
Q

What is adaptive /perihilar fsgs

Causes

A

When one kidney is diseased and other kidney develops hyperfiltration injury

RAS, REFLUX NEPHROPATHY MALIGNANCY
OBESITY SICKLE CELL ANEMIA

98
Q

Characteristics of primary fsgs

A 
75%  nephrotic syndrome
25%  microscopic hematuria proteinuria better prognosis 
Biopsy 
IF focal IgM +-C3 
EM more than 50% podocyte effaced
99
Q

Variant of FSGS

Which variant has better prognosis why

A

Tip variant best prognosis
Similar to MCD
Collapsing variant worst prognosis
CAUSED by hiv heroin pamidronate parvovirus

100
Q

Mgt of FSGS

A

Adult with nephrotic syndrome- (75%)
Steroids
1mg/kg/day given for 6-8 months

Adult with asymptomatic presentation(25%)
Acei arb and salt restriction

101
Q

How to treat resistance in fsgs

A

Resistance no response after 4 months

Treatment cyclosporin tacrolimus

Medicine (11 decks)

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