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Met 3b > Nephrotic Syndrome + Glomerulonephritis > Flashcards

Nephrotic Syndrome + Glomerulonephritis Flashcards

1
Q

Proteinuria

A

Represents abnormal glomerular filtration barrier function (as this is what is supposed to keep proteins out of urine)

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2
Q

Normal proteinuria

A

<150mg/day (around 30mg is albumin)

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3
Q

Microalbuminuria

A

30-300mg/day

ACR= 3-30mg/mmol

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4
Q

Macroalbuminuria

A

> 300mg/day

ACR= >30mg/mmol

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5
Q

Asymptomatic proteinuria

A

<3g/day

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6
Q

Nephrotic range proteinuria

A

> 3g/day

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7
Q

Proteinuria measurement- Urine Dipstick

A 
Trace= 15-30mg/dL
1+= 30-100mg/dL
2+= 100-300mg/dL
3+= 300-1000mg/dL
4+= >1000mg/dL
Will show up +ve if protein >300mg/day
Convenient and easy
Protein excretion not consistent throughout day
Only albumin detected
False negatives in multiple myeloma (protein component not albumin)
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8
Q

Proteinuria measurement- ACR/PCR

A

Daily creatinine excretion almost constant 910mmol/day)
Therefore ACR/PCR corrects for changes in urine conc. throughout day
First morning specimen most accurate
Can multiply PCR/ACR x 10 to obtain approx. value for 24hr excretion
Limitations- extremes of muscle mass, collection timing

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9
Q

24 hour urine collection- proteinuria

A

Gold standard
Impractical + difficult
Figure precise but often not necessary

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10
Q

Different causes of oedema- pathophysiological mechanisms

A

Increased hydrostatic pressure
Decreased oncotic pressure
Increased capillary permeability
Lymphatic blockage

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11
Q

Oedema- underfill hypothesis

A

Decrease in intravascular colloid oncotic pressure due to hypoalbuminuria
Leads to intravascular vol. depletions
Results in overactivation RAAS–> salt and water retention

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12
Q

Oedema- overfill hypothesis

A

Primary mechanism in nephrotic syndrome
Sodium retention is primary event due to increased Na/K ATPase activity in collecting duct
Leads to expansion of intravascular volume that increases hydrostatic pressure to force more fluid into interstitial space

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13
Q

Nephrotic syndrome

A

Clinical syndrome arising from failure of glomerular filtration barrier to restrict passage of proteins into Bowman’s space
Proteinuria (>3g/day) associated with hypoalbuminuria (<30g/L), generalised oedema, hyperlipidaemia + thrombotic tendency

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14
Q

Nephritic syndrome

A

Clinical syndrome associated with underlying glomerulonephritis (inflammation of glomerulus)
Haematuria, mild proteinuria, hypertension, impaired renal function, oliguria + mild oedema

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15
Q

Nephrotic syndrome diagnostic criteria

A

Proteinuria >3g/day
Hypoalbuminuria <30g/L
Generalised oedema
Hypercholesterolaemia

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16
Q

Nephrotic syndrome clinical history

A

Generalised oedema
Frothy urine
Collateral history- previous history, OTC NSAIDS, fam history renal disease, weight loss etc

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17
Q

Nephrotic syndrome Investigations

A

Exam- peripheral + sacral oedema, periorbital oedema, ascites, pleural effusions
BP- can be normal, low or raised
Urine dipstick- protein 4+, blood may be + or -

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18
Q

Nephrotic syndrome differential diagnoses

A 
Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Amyloidosis
Diabetic nephropathy
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19
Q

Minimal change disease- nephrotic syndrome

A

Most common cause nephrotic syndrome in children
Idiopathic
Secondary to- recent resp. infection, immunisation, NSAIDs, haematological malignancy
Massive oedema- facial + periorbital swelling, ascites, pleural + pericardial effusions
Absence of microscopic haematuria
BP= low/normal
Light microscopy= normal
Electron microscopy= effacement of podocyte end-feet
Treatment= corticosteroids

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20
Q

Focal segmental glomerulosclerosis- nephrotic syndrome

A

Most common cause in Hispanic + African American adults
Idiopathic
Secondary to- longstanding hypertension, any chronic kidney condition, HIV, heroin, obesity
Microscopic haematuria often present
BP often raised
Light microscopy- segmental sclerosis + hyalinosis
Electron microscopy- effacement of podocyte end-feet
Treatment- immunosuppression

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21
Q

Nephrotic syndrome- membranous nephropathy

A

Most common cause primary nephrotic syndrome in Caucasian adults
Most commonly idiopathic
Secondary to- drugs (gold, NSAIDs, penicillamine), infections (HBV, HCV, syphilis), SLE, solid tumours
Microscopic haematuria common
BP often raised
VTE common
Light microscopy- diffuse capillary + GMB thickening
Immunostaining- positive IgG staining
Electron microscopy- subendothelial deposit humps in GBM
Treatment- immunosuppression

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22
Q

Nephrotic syndrome- amyloidosis

A

Associated with chronic conditions that predispose amyloid deposition
e.g. AA amyloid in IV drug users

23
Q

Nephrotic syndrome- diabetic nephropathy

A

Light microscopy- mesangial expansion, GBM thickening, Kimmelstein-Wilson nodules
Electron microscopy= GBM thickening

24
Q

Nephrotic syndrome- Treatment of oedema

A

Restrict salt <2g/day
Fluid restriction <1l/day
Loop diuretics to decrease fluid retention

25
Q

Nephrotic syndrome- Reduction proteinuria

A

Will reduce aggravation of tubulointerstitial fibrosis which will reduce progression to functional decline
ACEI or ARB for anti-proteinuria effects
BP <125/70
Protein intake 0.8g/kg/day

26
Q

Nephrotic syndrome- Anticoagulation

A

NS risk factor for thrombosis

Anti-coagulate with SC heparin or warfarin for duration

27
Q

Nephrotic syndrome- Infection

A

Low IgG predisposes to infection
Treat infection promptly
Vaccinate against pneumococcus

28
Q

Nephrotic syndrome- Dyslipidaemia

A

Dietary restrictions

Statins

29
Q

Nephrotic syndrome- Immunosuppression, minimal change

A

1st line= corticosteroids
2nd line= CNI
3rd line= cyclophosphamide
4th line= rituximab

30
Q

Nephrotic syndrome- Immunosuppression, FSGS

A

1st line= corticosteroid
2nd line= CNI
3rd line= cyclophosphamide
4th line- MMF

31
Q

Nephrotic syndrome- Membranous

A

1st line= corticosteroid + calcineurin inhibitor
2nd line= cyclophosphamide
3rd line= MMF
4th line= Rituximab

32
Q

Nephritic syndrome (Glomerulonephritis) diagnostic criteria

A

Haematuria (urine dip +++)
Red cell casts on urinary microscopy
Mild proteinuria (<1-1.5g/day)
With progression –> hypertension, oedema, AKI

33
Q

Glomerulonephritis- immune mediated

A

IgA nephropathy (berger disease)–> most common cause GN worldwide
Small vessel vasculitis- Wegener’s granulomatosis, microscopic polyangiitis
Systemic lupus
Anti-GBM disease
Cryoglubinaemia

34
Q

Glomerulonephritis- infections

A

Viral –> hep B, hep C, HIV
Post-streptococcal
Subacute bacterial endocarditis

35
Q

Glomerulonephritis malignancy

A

Myeloma

Lymphoma

36
Q

Glomerulonephritis- IgA nephropathy

A

Episodic gross haematuria that occurs concurrently with resp/GI infections
Mesangial proliferation
Young adults
Purpuric skin rash
Arthritis
Abdo pain
Worse prognosis if increased BP, male, proteiuria

37
Q

Glomerulonephritis- Anti-GBM (Goodpasture’s disease)

A

Isolated renal and pulmonary effects
Anti-GBM in circulation/kidney
Treat- plasma exchange, steroids, cytotoxics

38
Q

Glomerulonephritis- Wegener’s (granulomatosis with polyangitis)

A 
Vasculitis rash
Sinusitis
Epistaxis
Haemoptysis
Eye redness
39
Q

Glomerulonephritis- microscopic polyangitis

A 
Vasculitis rash
Haemoptysis
Eye redness
Diarrhoea + abdo pain
Neuropathy
40
Q

Glomerulonephritis- SLE

A

Butterfly malar rash
Painful + swollen joints
Fever
Chest pain

41
Q

Glomerulonephritis- Myeloma

A 
Bone pain
Fractures
Anaemia
Repeated infections
Easy bleeding
42
Q

Glomerulonephritis- Post-streptococcal

A 
Occurs around 2 weeks after infection
Oedema
Headache
Oliguria
Fever
Malaise
Nausea
43
Q

Glomerulonephritis Investigations- bloods

A 
FBC
U+Es
LFTs 
CRP
Nephritic screen
44
Q

Rapidly Progressive Glomerulonephritis

A

Term used to describe rapid loss of renal function (50% GFR decline in 3 months) associated with formation of epithelial crescents in majority of glomeruli
Increased creatinine and decreased GFR secondary to GN

45
Q

Rapidly Progressive Glomerulonephritis- biopsy

A

Crescent moon shape consisting of fibrin + plasma proteins (e.g. C3b) with glomerular parietal cells, monocytes, macrophages

46
Q

Rapidly Progressive Glomerulonephritis- types

A

Immune complex RPGN
Pauci-Immune RPGN- 80-90% are ANCA positive
Anti-GBM

47
Q

Rapidly Progressive Glomerulonephritis- treatment

A

Corticosteroids

Cyclophosphamide

48
Q

Pulmonary renal syndrome

A

Pulmonary haemorrhage occurring simultaneously with GN
Dyspnoea, cough, fever, haemoptysis, peripheral oedema, haematuria
Treatment= corticosteroids, cyclophosphamide, plasma exchange

49
Q

Glomerulonephritis treatment- oedema

A

Limit salt <5g
Limit fluid <1L
Diuretics (loop)

50
Q

Glomerulonephritis treatment- proteinuria

51
Q

Glomerulonephritis treatment- BP

A 
<130/80
Diruretics
BB
CCBs
ACEI/ArB
52
Q

Glomerulonephritis treatment- immunosuppression

A 
Corticosteroids
Cyclophosphamide
Calcineurin inhibitors
Azathioprine
Mycophenoate
Rituximab
53
Q

Factors that indicate poor prognosis with any glomerulonephritis

A

Heavy proteinuria
Sever hypertension
Significant elevations creatinine

Met 3b (21 decks)

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