Nephrotic Syndrome Flashcards

1
Q

What constitutes as remission for nephrotic disease?

A

3 days dipstick -ve for proteins (?)

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2
Q

Make sure to cover hsp and it’s extrarenal manifestations

A

GI Bleed
Glomeurlonepgritis
Abdo sepsis
Intrsusseption

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3
Q

What are the causes of increased interstitial fluid?

A

Poor lymph drainage:
Lymphoedema - Congenital vs Physical/blockage

Poor venous drainage + pressure:
Venous obstruction
E.g. venous thrombosis

Low oncotic pressure - low albumin/protein:
Malnutrition
Decreased production - Liver disease

Increased loss:
Gut
Kidney - Nephrotic syndrome

Salt and water retention:
Kidney - impaired GFR
Heart failure

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4
Q

What symptoms characterise nephrotic syndrome?

A
Hypoalbuminaemia 
->
Proteinuria (heavy)
->
Oedema 
\+
Hyperlipidaemia (from reactive hepatic protein synthesis, including of lipoproteins)

(depending on the cause/types of protein lost, may also be other complications e.g. infection, thrombosis)

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5
Q

How do you test for heavy proteinuria?

A
Semi-quantitative = Dipstick: 
Negative-trace = 0-30mg/dL 
1+ = 30-100mg/dL
2+ = 100-300mg/dL
3+ = 300-1000mg/dL
4+ = >1000mg/dL 
3-4 = increased likelihood of hypoalbuminaemia 

Quantitative = First morning urine: Protein:creatinine
Normal = <20mg/mmol
No definite level that means its nephrotic but >600mg/mmol is likely to produce hypoalbuminaemia (although can occur at lower levels)

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6
Q

What is hypoalbuminaemia?

A

Normal albumin range = 35-45g/L

Hypo = <25-30g/L – this level usually associated with fluid retention and oedema

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7
Q

What characterises the oedema?

A

Pitting

Gravitational e.g. shifting dullness

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8
Q

What is hyperlipidaemia?

A

Normal lipid range = 100-129mg/dL

Hyper = 160-189mg/dL

Arises due to the low serum oncotic pressure which then leads to reactive hepatic protein synthesis including lipoproteins

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9
Q

What are the different types of nephrotic syndrome?

A

Congenital - <1yr

Steroid sensitive NS (SSNS)

Steroid resistant NS (SRNS)

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10
Q

What are the clinical features of steroid sensitive NS?

A

Normal BP

No macroscopic haematuria

Normal renal function

No features to suggest nephritis

Respond to steroids

Histology – “minimal change” usually

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11
Q

What are the clinical features of steroid resistant NS?

A

Elevated BP

Haematuria

May be impaired renal function

Features may suggest nephritis

Failure to respond to steroids

Histology – various: underlying glomerulopathy, basement membrane abnormality

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12
Q

What is the epidemiology of different nephrotic syndromes? (general)

A

Most common age 1-15yrs = minimal change disease – 85-40% (decreases with age)

Focal segmental glomerulosclerosis – makes up about 20% of the cases between ages 10-15rys

Other causes – mesangiocapillary glomerulonephritis etc make up about 30-40% total age 10-15yrs

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13
Q

What is the epidemiology of steroid sensitive nephrotic syndrome? (mostly minimal change)

A
Peak incidence age 2-5yrs 
M>F 
Greater incidence in Asian populations 
Recurrent relapse + 5% continue into adult life 
Potential immunological aetiology 

Normal renal function if treated with steroids

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14
Q

How do you treat SSNS?

A

First episode:
Admission
If ?septic - treat as such

Address oedema - Na/water moderation, diuretics (furosemide), IV albumin

Steroid therapy - prednisolone 60mg/m2 OD for 4 weeks then 40mg/m2 alternate days for 4 weeks

Complication prophylaxis - phenoxymethylpenicillin (Pen v), measles + varicella + pneumococcal vaccination

Relapse = protienuria of 3+ on 3 consecutive days - prompts restarting of prednisolone

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15
Q

What is a common renal cause of AKI and how does it present?

A

Acute glomerulonephritis:

Haematuria – often macroscopic

Proteinuria – variable amounts

Impaired GFR – rising creatinine (variable)

Salt and water retention – hypertension and oedema

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16
Q

What is acute post-streptococcal glomerulonephritis?

A

Follows a nasopharyngeal or skin infection

Often group A beta-haemolytic strep infections – nephritogenic strains

Antigen-antibody complexes deposit in the glomeruli and result in complement system activation and subsequent inflammation

Presents c.10days+ post infection – initially with haematuria, swelling, decreased urine output then HTN and signs of CV overload

17
Q

How do you investigate post-streptococcal glomerulonephritis?

A

Bloods:
FBC – mild, normochromic, normocytic anaemia
U+E – increased urea + creatinine; possible hyperkalaemia + metabolic acidosis
Immunology – raised antistreptolysin O (ASO) (raised - >200units/ml - after strep infections), antiDNAse B (antibodies to protein produced by group A strep), low complements – C3 + C4

Urinalysis:
Haematuria – often macroscopic
Proteinuria – dipstick elevation
Microscopy – RBC casts (WBC casts may indicate tubular disease including acute pyelonephritis)

Swabs:
Throat, nasal, skin etc - for the strep infection itself + MC+S

18
Q

How is post-streptococcal glomerulonephritis managed?

A

Penicillin:
Treat the strep infection (if still ongoing)

Fluids:
Monitor input/output, ?catheter
Fluid + salt restriction

Diuretics:
For fluid balance and HTN

Correct any electrolyte imbalances – K, acidosis etc.

Possible dialysis if necessary (rare)

19
Q

What is the prognosis of acute post-streptococcal glomerulonephritis?

A

95% full recovery + no long term impact on renal function

Non-recurrent

20
Q

What is Henoch-Schonlein Purpura (HSP)?

A

Aka IgA vasculitis - involving skin, joints, gut and kidneys

IgA deposition in the glomerulus = IgA nephropathy (Berger’s disease)

More common in young adults - 16-35

Symptoms usually begin 1-2 days post URTI (unlike the post-strep = weeks)

Possible renal symptoms: 
Haem/proteinuria 
Nephrotic syndrome 
Acute nephritis 
Renal impairment 
HTN 

Skin/MSK symptoms:
Petechial, mostly buttocks and extensor surfaces of arms and legs
Swollen, painful knees and ankles

Steroid resistant – may need immunosuppression

Variable prognosis – can end up with end stage renal disease (ESRD) + dialysis