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Nephrology > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

etiology of GN

A
  1. Primary- idiopathic
    2.Secondary
    DM, SLE, CTdisease, Amyloidosis,
    Infection(Hep B,Malaria),
    Drugs(Penicillin,Gold,penicillamine)
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2
Q

Sx of injury to glomeruli

A

Proteinuria
hematuria
uremia
oliguria
edema
increased BP

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3
Q

Cause of proteinuria

A

increased capillary permeability

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4
Q

cause of hematuria

A

rupture of capillary walls

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5
Q

cause of uremia

A

reduced Glomerular filtration

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6
Q

cause of oliguria

A

reduced urine production

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7
Q

cause of edema

A

increased Na+ and water retention

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8
Q

cause of increased BP

A

disturbance of RAAS

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9
Q

clinical presentation of GN

A

 Urinary abnormalities – proteinuria,
haematuria
 Acute nephritic syndrome
 Nephrotic syndrome
 Rapidly progressing /ARF
 CRF
 Mixed picture of above

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10
Q

Nephrotic syndrome proteinuria levels

A

> 3.5g/d

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11
Q

can proteinuria get associated with hematuria in GN

A

Yupsiee

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12
Q

hematuria with albuminuria is highly suggestive of

A

GN

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13
Q

what should be ruled out if hematuria presents alone

A

urological causes

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14
Q

signs of hematuria which suggests glomerular bleeding

A

presence of RBC casts
dysmorphic figures

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15
Q

Nephrotic syndrome is characterized by

A

Proteinuria (heavy) 3.5 g/1.73 m2 S.A
Hypoalbuminaemia (<2.5 g/dl)
Oedema
Hyperlipidaemia(increased LDL, VLDL,
IDL)

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16
Q

causes of GN

A

Primary - idiopathic
Secondary- autoimmund disorders (SLE), diabetic nephropathy, drugs ( gold, penicillamine), infections, malignancy

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17
Q

common malignancies associated with GN

A

colorectal CA
Bronchial CA

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18
Q

HIstological types of GN

A

Minimal change disease (25-50%)
Membranous glomerulonephritis (1-
25%)
Focal and segmental glomerulosclerosis
(25%)
Proliferative glomerulonephritis (25%)

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19
Q

characteristics of edema seen in GN

A

initially dependant pitting
oedema (puffy eyes, swollen legs), later
becomes generalised (ascites, pleural
effusion, scortal edema)

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20
Q

elevated BP is common in nephrotic syndrome (T/F)

A

false. uncommon. reflex HTN is possible

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21
Q

Dx of Nephrotic syndrome

A

o Urine analysis
 +3 or +4 proteinuria
 microscopic haematuria
 hyaline, granular casts.
o Serum albumin (< 2.5 g/dl)
o Serum cholesterol, triglycerides & total
lipids
o Blood urea & Serum creatinine
o 24 hr urine protein excretion > 3g/day
o Urine & serum electrophoresis
o Investigations for underlying cause –
ANF, dsDNA, other Ab (ANCA, antiGBM), DM, Multiple myeloma, for
infection (ASOT, Malarial parasite)
o Serum C3 levels
o Biopsy (Indications - Steroid resistant
nephrotic syndrome, Persistent
hypertension and/or haematuria

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22
Q

Mx of nephrotic Syndrome

A

 Diet
o low salt
o normal protein diet
o low fat
 Symptomatic treatment of oedema
o diuretics - K+ sparing diuretics, Loop
diuretics, sometimes with thiazides
o plasma (vol. depleted, no response to
diuretics)
 Other measures to reduce proteinuria -
ACEI ,NSAIDs
 Lipids - statins(Cardiovascular dx –
increased risk due to hyperlipidaemia)
 Treat specific glomerular disease
 Treat complications - infections
(peritonitis, cellulitis, UTI,LRTI)

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23
Q

Minimal change GN appearance on Microscope

A

look nearly normal

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24
Q

Colour and appearance of kidneys

A

Yellowish (lipid nephrosis)

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25
Q

cells of PCT and appearance of foot processes

A

laden with lipid- PCT
foot processes- fused

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26
Q

etiology of MCGN

A

T- cell disorders
associated with atopy and viral infections
Secondary to drugs (NSAID, Li, ABx)
associated with HCV, HIV, TB

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27
Q

Complications of Minimal change GN

A
  1. Infection
    ↑ Susceptibility during a relapse
    ↓ Immunoglobulins
    ↓ Factor B
    Oedema fluid good culture medium
    Peritonitis – most frequent
    Strep. pneumoniae – most common
    organism
    Other infections – UTI, pneumonia,
    cellulitis
  2. Thrombosis- increased venous
    thrombosis
    ↓ Anti thrombin III
    ↑ Fibrinogen
    Risk greatest when serum albumin is very low
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28
Q

Relapse of MCGN

A

> 3 days of >3+ urine protein,
associated with oedema

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29
Q

Spontaneous remission towards the end of
second decade in MCGN (T/F)

A

True

30
Q

what might influence the course of the disease in MCGN

A

the duration of treatment

31
Q

Mx of MCGN

A

Oral prednisolone

32
Q

FSGN affects

A

certain segments of some not all glomeruli

33
Q

Sx of FSGN

A

Massive proteinuria/haematuria/HT/renal
impairment

34
Q

etiology of FSGN

A

o Primary idiopathic disease
o In association with HIV( collapsing
FSGS) and heroin addiction
o As a secondary event in other forms of
GN- e.g. IGA nephropathy
o As a component of glomerular ablation
nephropathy
o HT, sickle nephropathy, obesity

35
Q

FSGN responds to steroids (T/F)

A

False. resistant to steroids

36
Q

Membranous GN EM findings

A

Diffuse thickening of the GCBM
Silver stains show spike and dome appearance

37
Q

Etiology of Membranous GN

A

o Idiopathic
o Infections- chronic hepatitis B, syphilis,
schistosomiasis, malaria
o Malignant epithelial tumours- colon,
lung, lymphoma, leukaemia
o SLE(class V disease),
o Exposure to organic salts- gold, mercury
o Drugs- penicillamine, captopril
o Metabolic disorders- diabetes,
thyroiditis

38
Q

Mx of Membranous GN

A

combination of
corticosteroid+ another agent
BP control- ACEI reduce proteinuria
Consider anticoagulation

39
Q

prognosis of Membranous GN

A

 One – third – spontaneous remission
 One third – remain proteinuric
 One third- develop ESRF

40
Q

clinical features of acute nephritic syndrome

A

o oedema- periorbital, generalized (mild -
moderate), less marked than in
Nephrotic synd.
o oliguria - UOP <700ml/day
o haematuria (microscopic-macroscopic)
o hypertension
o Circulatory overload (increased JVP,
orthopnoea, 3rd HS, bilateral basal
crepitations)
o Renal impairment
o Elevated blood urea & serum creatinine

41
Q

causes of acute nephritic syndrome

A

o Idiopathic - Less common
o Secondary - Post streptococcal
Glomerulonephritis is the commonest
cause

42
Q

Pathophysio of acute nephritic syndrome

A

inflammatory damage
to filtration surface, shunting the blood
(glomerular haematuria) → reduced GFR
(Uraemia) → reduced filtrate volume →
reduced distal delivery, constant or
increased Na+ absorption, critical sodium
intake → positive sodium balance →
intravascular volume increase (oedema,
increased CO, hypertension, CCF)

43
Q

acute nephritic syndrome findings

A

Skin/ throat sepsis +
Edema Mild/ moderate
Hematuria Macroscopic(often), microscopic
Oliguria +
HTN +
Renal impairment +/-
Circulatory overload +

44
Q

Nephrotic syndrome

A

Skin/ throat sepsis -
Edema severe
Hematuria +/-
Oliguria -
HTN +/-
Renal impairment +/-
Circulatory overload -

45
Q

Ix and findings of acute nephritic syndrome

A

o Urine microscopy- RBC, RBC casts, WBC,
protein (1 - 2 + on heat test)
o Blood urea, Serum creatinine - elevated
o Creatinine clearance (GFR) - reduced
o CXR
o For the underlying cause – eg ASOT

46
Q

course and prognosis of acute nephritic syndrome

A

acute nephritic syndrome can lead to 1. acute renal failure, HT encephalopathy, pulmonary edema
2.Asx, hematuria +/- proteinuria
3. well

1.acute renal failure, HT encephalopathy, pulmonary edema
2.Asx, hematuria +/- proteinuria can lead to either CRF, death

47
Q

Mx of acute nephritic syndrome

A

o Monitor - UOP, Weight, BP ,
Macroscopic Haematuria, BU, SE (esp if
ARF)
o Treatment of Strep. Infection -Penicillin
o Fluids - if oliguria - 500 cc + previous
days UOP
o Diet - salt restriction, K+ restriction,
+/- protein reduction to 20g/d if BU is
high
o Diuretics
o Anti- hypertensives
o Treatment of complications (Sometimes
dialysis needed)
 LVF
 ARF
 Hypertensive encephalopathy

48
Q

Acute proliferative GN aka

A

Post streptococcal GN

49
Q

When does PSGN occur

A

Occurs 1-3 weeks after a group A beta
haemolytic streptococcal infection.(throat
infection/ cellulitis/ otitis media)

50
Q

PSGN happens only with certain nephritogenic strains (T/F)

A

True

51
Q

Most cases of the intial infections of PSGN

A

pharyngitis or a skin infection

52
Q

PSGN EM findings

A
  1. Glomerulus is enlarged and cellular. 2.Proliferation and swelling of mesangial and
    endothelial cells
53
Q

types of cells that are involved in PSGN

A

Infiltration by neutrophils and monocytes

54
Q

UOP for a person who comes with renal failure

A

Last day UOP + 400cc ( to cover insensible fluid loss)
but the patient will not know how much is the last UOP is, so monitor the patient’s UOP for 1 hour and 30cc

55
Q

characterstic finding of membranoproliferative GN

A

double contour or tram track appearance with silver or PAS

56
Q

etiology of membrano proliferative GN

A

o Idiopathic
o Type 1 picture may be seen in SLE,
hepatitis B & C, infected AV shunts,
secondary infections, malignancies

57
Q

The emergency GN condition

A

Crescentic (Rapidly Progressing) GN

58
Q

what happens in Crescentic (Rapidly Progressing) GN

A

rapid and progressive loss
of renal function associated with severe
oliguria

59
Q

how are crescents formed in RPGN

A

proliferation of
parietal epithelial cells and infiltration by
monocytes and macrophages

60
Q

classification of RPGN

A

Type 1 - anti GBM disease, linear deposits of IgG
eg- 1.Goodpasture’s syndrome
2. Idiopathic anti GBM mediated

Type 2- - Immune complex
mediated disease
 Granular deposits of IgG
 Post streptococcal, SLE, IgA
nephropathy, HSP

Type 3 - pauci immune type
 Systemic vasculitis like polyarteritis
nodosa or Wegener’s granulomatosis

61
Q

IgA Nephropathy occurs after….

A

within 1-2 days of a
non-specific URTI

62
Q

Sx of IgA nephropathy

A

Recurrent macroscopic or microscopic
haematuria

63
Q

Serum IgA levels in IgA nephropathy

A

raised by 50%

64
Q

EM findings of IgA nephropathy

A
  • Mesangial deposits of IgA.
  • Glomerular injury due to activation of
    alternate complement pathway.
  • Mesangial proliferation, focal proliferative
    GN or rarely crescentic GN.
65
Q

diseases associated with IgA nephropathy

A

HSP, CLCD, coeliac dx, CA
bronchus, sero negative spondyloarthritis

66
Q

difference between IgA nephropathy and PSGN

A

IgA - 1-2 days after infection, relapses
PSGN- 10 days after, no relapses

67
Q

Spot test done on nephrotic syndrome

A

UPCR ( urine protein creatinine ratio)

68
Q

GN classification

A

Divided mainly into 2
1. minimal change Disease
100% clincal picture is nephrotic syndrome
good response to steroids
onset in children

  1. non minimal change disease
    This is divided into two again.
    A. Non- proliferative GN ( mostly nephrotic picture )
    Eg- membranous GN
    FSGN
    glomerulosclerosis
    B. Proliferative GN ( mostly nephritic)
    Acute diffuse proliferative GN
    Membranoproliferative GN
    Mesangioproliferative GN
    RPGN
69
Q

Abdominal pain in nephrotic syndrome patient

A

Spontaneous bacterial peritonitis
Renal vein thrombosis
Hypovolemia causing gut ischemia
Gastritis ( steroids given )

70
Q
A

Nephrology (4 decks)

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