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Year 3 - Met3b > Nephrotic Syndrome > Flashcards

Nephrotic Syndrome Flashcards

1
Q

What is the diagnosis for nephrotic syndrome

A
  • Proteinuria > 3g/24hr
  • Hypoalbuminaemia <30g/dL
  • Oedema
  • Raised cholesterol
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2
Q

What is the mechanism of proteinuria

A
  • Primary renal disease
  • secondary caused

The normal physiolgoical asepcts of the bowmans capsule are disrupted which allow protein to leak through

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3
Q

Why dont we develop protienuira as a normal individual

A
  • fenestrated endothelium of the capillaries
  • basmenet membrane
  • epithelial of the bowmans capsule - podocytes
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4
Q

What is the main protein in proteinuria/ glomuerular nephrotic syndrome

A

albumin

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5
Q

How do you assess proteinuria

A

Urine dipstick

24 hour urine collection

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6
Q

What is the gold standard for assessing proteinuria

A

24 hour urine collection

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7
Q

What does the urine dipstick test tell you

A
  • tells you that protein is presnet
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8
Q

Name the levels of proteinuria

A 
Negative
Trace — between 15 and 30 mg/dL 
1+ — between 30 and 100 mg/dL
2+ — between 100 and 300 mg/dL 
3+ — between 300 and 1000 mg/dL 
4+ — >1000 mg/dL
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9
Q

what concentration of substance is constant

A

creatine is constant irrespective of health and disease

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10
Q

How do you measure protein excretion with just a sample of urine

A
  • Use the protein creatine ratio (PCR)
  • Creatine remains constant irrespective of health and disease
  • can be used to measure protein
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11
Q

How many grams a day of protein is 100mg/mmol

A

Urine PCR 100mg/mmol = 1g/24hour

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12
Q

How many grams of protein is supposed to be passed a day

A

3g/24hour

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13
Q

what are the two hypothesis as to why patients with nephrotic syndrome develop oedema

A
  • Underfill hypothesis

- Overfill hypothesis - thought to be the predominant reasons why they get oedema

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14
Q

Describe underfill hypothesis (oedema development in nephrotic syndrome)

A
  • Decrease in intravascular colloid osmotic pressure due to low serum albumin - Intravascular volume depletion
  • Activation of the renin angiotensin system and retention of salt and water
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15
Q

Describe overfill hypothesis (oedema development in nephrotic syndrome)

A

Primary sodium retention

  • due to the predominant mechanism of oedema in nephrotic syndrome, heart failure and liver failure
  • as you retain sodium in the kidneys you thus retain water
  • this means that water follows sodium into the intravascular compartment and this then moves into the extravascular compartment
  • when the extravascular compartment expands, ANP is released to excrete water but ANP resistance develops
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16
Q

Describe how normal transcapillary oncotic pressure gradient works

A
  • starlings law - mentions that it is the net between the hydrostatic and oncotic pressure that drives fluid movement between the inter vascular and interstitial compartments on the body
  • Hydrostatic pressure is driven by the cardiovascular system
  • hydrostatic pressure decreases as you go from the arterial end to the venous end
  • the hydrostatic pressure in the interstitial compartment stays consent
  • so the net hydrostatic pressure on the arterial end will drive fluid out whereas on the venous end it will drive fluid back in
  • sodium is driven into the intravascular compartment
  • water follows
  • venous end fluid is pushed in
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17
Q

What is colloid osmotic pressure generated by

A

driven by negatively charged proteins in both the intervascular and interstitial compartments

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18
Q

What is the transcapillary oncotic pressure gradient

A
  • Is the difference between the intravascular and interstitial COP
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19
Q

What does starlings law say

A
  • mentions that it is the net between the hydrostatic and oncotic pressure that drives fluid movement between the inter vascular and interstitial compartments on the body
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20
Q

Describe the mechanism of action of nephrotic syndrome

A
  • you loose colloid osmotic pressure due to lack of albumin and total protein in the intervascular
  • therefore the colloid osmotic pressure exceeds the transcapillary hydrostatic pressure leading to retention of salt and water
  • this leads to intravascular volume depletion
  • activation of the RAAS
  • leading to further water and salt retention
21
Q

What is likely to be the predominant mechanisms for oedema in nephrotic syndrome

A

Overfill system

22
Q

in a urine dip what is the presentation of nephortic syndrome

A
  • protein

- in some cases blood

23
Q

What investigations should you do in nephrotic syndrome

A

Urine

  • protein/creatine raito
  • microscopy (to rule out infection)

Blood investigations

FBC, clotting (may need a biopsy), urea and electrolytes
LFTs ( check for serum albumin result)

imaging
- US renal tract before biopsy

Renal biopsy

24
Q

Name the primary and secondary causes of nephrotic syndrome

A

Primary

  • Minimal change disease
  • focal segmental glumerulosclerosis
  • Membranous nephropathy

Secondary

  • Diabetic nephropathy
  • lupus nephritis
  • pre-eclampsia
  • amyloid
  • congential nephropathy
25
Q

Without a renal biopsy you cannot determine

A

type of nephrotic syndrome

26
Q

What are the three most commonest nephrotic syndromes

A
  • Minimal change disease
  • focal segmental glumerulosclerosis
  • Membranous nephropathy
27
Q

What is the commonest cause of nephrotic syndrome in children

A
  • Minimal change disease
  • 90% of all NS in children <10y
  • 50% of all NS in children >10y
  • probablity is so high often they will not have a renal biopsy
  • causes 25% of adult nephrotic syndrome
28
Q

name the microscopic signs of minimal change disease as a nephrotic syndrome

A
  • Light microscopy is nealry identical to a normal glomeruli
  • effacement of the podocytes is the only positive findings in the histology
  • no microscopic haematuria - but this could be present in adults
29
Q

What is the only positive microscopy that indicates minimal change disease

A
  • effacement of the podocytes is the only positive findings in the histology
30
Q

Describe focal segmental glomerulosclerosis

A

Focal - not all glomeruli are affected

Segmental - part of the glomeruli are sclerosed

31
Q

Who is membranous nephropathy common in

A
  • Non diabetic adults
  • age (older)
  • male
  • caucasian
32
Q

describe the features of membranous nephropathy

A
  • Thickened capillary loops

- Subepithelial immunoglobulin deposition

33
Q

What is the causes of membranous nephropathy

A
  • autoimmune
  • malignancy: lung, breast, GI, prostate, haematological
  • Infection: hepatitis, streptococcus, malaria
  • immunological disease: SLE, rheumatoid arthritis, sarcoidosis
  • Drugs - penicillamine, gold
34
Q

How do you diagnose membranous nephropathy

A
  • Anti-phopsholipase A2 receptor antibody in 70-80% of idiopathic disease
  • diffusely thickened GBM due to sub epithelial depostis
35
Q

What are the complications of nephrotic syndrome

A
  • Infection (in children)
  • Thromboembolism
  • Renal Impairment
  • Dyslipidaemia
36
Q

How do you manage patients with nephrotic syndrome

A

• Treatment of Oedema - via fluid and salt restriction, or loop diuretics - aim for 0.5-1kg of weight loss per day

Treat underlying cause

  • adults need renal biopsy
  • then give treatment to induce remission such as corticosteroids in minimal change disease

• Reduction of proteinuria
- ACE/ARB to reduce proteinuria

  • Statins for dyslipidaemia
  • Anti-coagulation to prevent thromboembolism
  • Immunisation
  • Nutrition
37
Q

How can patients loose there oedema

A
  • restriction of fluids
  • 1 L day
  • Diuretics - go from loop diuretics, then to thiazide and then to aldosterone antagonists
38
Q

How do you reduce proteinuria

A
  • ACE inhibitors
  • Angiotensin receptor blockers
  • they work by reducing the intraglomerular pressure
  • Treat the cause
39
Q

What is the presentation of someone with nephrotic syndrome

A
  • generalised
  • pitting oedema which can be rapid and severe
  • pulmonary oedema
40
Q

Why do you get hyperlipidaemia in nephrotic syndrome

A
  • increase in cholesterol, LDL, triglycerides and decrease in HDL due to hepatic synthesis in response to decrease in oncotic pressure and defective lipid breakdown
41
Q

What can cause minimal change disease

A
  • idiopathic
  • association with drugs (NSAIDs, lithium)
  • paraneoplastic - haematological malignancy, usually Hodgkin’s lymphoma
42
Q

What is the treatment for minimal change disease

A
  • prednisolone 1mg/kg for 4-16 weeks

- can relapse

43
Q

What can cause focal segmental glomerulosclerosis

A
  • primary - idiopathic

- Secondary - HIV, heroin, lithium, lymphoma

44
Q

How do you treat focal segmental glomerulosclerosis

A
  • ACE/ARB and blood pressure control
  • corticosteroids only in primary idiopathic disease - remission in 25%, partial remission in up to 50%
  • Calcineurin inhibitors considered 2nd line
45
Q

How do you treat membranous nephropathy

A
  • ACE/ARB and blood pressure control

- immunosuppression only in those at high risk of progression

46
Q

What are the complications of nephrotic syndrome

A
  • Susceptibility to infection
  • thromboembolism
  • dyslipidaemia
  • renal impairment
47
Q

Why is there an increase risk of thromembolism

A
  • due to an increase in clotting factors, decrease in anti-thrombin III and platelet abnormalities
48
Q

How can amyloid lead to nephrotic syndrome

A
  • pathological folding of proteins leading to extracellular accumulation and organ dysfunction
49
Q

How do you treat membraneous nephropathy

A

Treatment

  • ACE/ARB
  • Blood pressure control
  • Immunosuppression – corticosteroids plus cyclophosphamide only in those at high risk of progression

Year 3 - Met3b (26 decks)

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