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Glomerulonephritis Flashcards

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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
cells of PCT and appearance of foot processes
laden with lipid- PCT foot processes- fused
26
etiology of MCGN
T- cell disorders associated with atopy and viral infections Secondary to drugs (NSAID, Li, ABx) associated with HCV, HIV, TB
27
Complications of Minimal change GN
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
28
Relapse of MCGN
> 3 days of >3+ urine protein, associated with oedema
29
Spontaneous remission towards the end of second decade in MCGN (T/F)
True
30
what might influence the course of the disease in MCGN
the duration of treatment
31
Mx of MCGN
Oral prednisolone
32
FSGN affects
certain segments of some not all glomeruli
33
Sx of FSGN
Massive proteinuria/haematuria/HT/renal impairment
34
etiology of FSGN
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
FSGN responds to steroids (T/F)
False. resistant to steroids
36
Membranous GN EM findings
Diffuse thickening of the GCBM Silver stains show spike and dome appearance
37
Etiology of Membranous GN
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
Mx of Membranous GN
combination of corticosteroid+ another agent BP control- ACEI reduce proteinuria Consider anticoagulation
39
prognosis of Membranous GN
 One – third – spontaneous remission  One third – remain proteinuric  One third- develop ESRF
40
clinical features of acute nephritic syndrome
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
causes of acute nephritic syndrome
o Idiopathic - Less common o Secondary - Post streptococcal Glomerulonephritis is the commonest cause
42
Pathophysio of acute nephritic syndrome
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
acute nephritic syndrome findings
Skin/ throat sepsis + Edema Mild/ moderate Hematuria Macroscopic(often), microscopic Oliguria + HTN + Renal impairment +/- Circulatory overload +
44
Nephrotic syndrome
Skin/ throat sepsis - Edema severe Hematuria +/- Oliguria - HTN +/- Renal impairment +/- Circulatory overload -
45
Ix and findings of acute nephritic syndrome
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
course and prognosis of acute nephritic syndrome
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
Mx of acute nephritic syndrome
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
Acute proliferative GN aka
Post streptococcal GN
49
When does PSGN occur
Occurs 1-3 weeks after a group A beta haemolytic streptococcal infection.(throat infection/ cellulitis/ otitis media)
50
PSGN happens only with certain nephritogenic strains (T/F)
True
51
Most cases of the intial infections of PSGN
pharyngitis or a skin infection
52
PSGN EM findings
1. Glomerulus is enlarged and cellular. 2.Proliferation and swelling of mesangial and endothelial cells
53
types of cells that are involved in PSGN
Infiltration by neutrophils and monocytes
54
UOP for a person who comes with renal failure
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
characterstic finding of membranoproliferative GN
double contour or tram track appearance with silver or PAS
56
etiology of membrano proliferative GN
o Idiopathic o Type 1 picture may be seen in SLE, hepatitis B & C, infected AV shunts, secondary infections, malignancies
57
The emergency GN condition
Crescentic (Rapidly Progressing) GN
58
what happens in Crescentic (Rapidly Progressing) GN
rapid and progressive loss of renal function associated with severe oliguria
59
how are crescents formed in RPGN
proliferation of parietal epithelial cells and infiltration by monocytes and macrophages
60
classification of RPGN
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
IgA Nephropathy occurs after....
within 1-2 days of a non-specific URTI
62
Sx of IgA nephropathy
Recurrent macroscopic or microscopic haematuria
63
Serum IgA levels in IgA nephropathy
raised by 50%
64
EM findings of IgA nephropathy
* Mesangial deposits of IgA. * Glomerular injury due to activation of alternate complement pathway. * Mesangial proliferation, focal proliferative GN or rarely crescentic GN.
65
diseases associated with IgA nephropathy
HSP, CLCD, coeliac dx, CA bronchus, sero negative spondyloarthritis
66
difference between IgA nephropathy and PSGN
IgA - 1-2 days after infection, relapses PSGN- 10 days after, no relapses
67
Spot test done on nephrotic syndrome
UPCR ( urine protein creatinine ratio)
68
GN classification
Divided mainly into 2 1. minimal change Disease 100% clincal picture is nephrotic syndrome good response to steroids onset in children 2. 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
Abdominal pain in nephrotic syndrome patient
Spontaneous bacterial peritonitis Renal vein thrombosis Hypovolemia causing gut ischemia Gastritis ( steroids given )
70

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