Glomerular disease: nephrotic syndrome Flashcards

1
Q

Diagnostic criteria for glomerulonephritis

A
  • proteinuria >3g/day
  • hypoalbuminaemia <30g/dL
  • oedema
  • raised cholesterol
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2
Q

Mechanism of proteinuria

A
  • glomerular structure
  • basement membrane = podocytes + collagenous membrane + endothelial cells
  • disrupted in nephrotic syndrome so proteins (mostly albumin) can get through
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3
Q

Assessment of proteinuria

A
  • urine dipstix (all patients routine)
  • get blood, protein, leukocytes, nitrites and pH from this
  • simple bedside test
  • protein = negative, trace, 1-4
  • 24 hour urine collection is gold standard but practically not reliable
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4
Q

Dipstix protein results

A
Negative
trace = 15-30 mg/dL
1+ = 30-100 mg/dL
2+ = 100-300 mg/dL
3+ = 300-1000 mg/dL
4+ = >1000mg/dL
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5
Q

Protein/creatinine ratio

A
  • daily creatinine excretion constant = 1000mg/8.8mmol per day
  • so do PCR
  • normal PCR 100mg/mmol/1g/day
  • nephrotic syndrome = 3g/day so 300mg/mmol
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6
Q

Why do patients get oedema in nephrotic syndrome?

A

UNDERFILL HYPOTHESIS

  • best understood
  • decrease in intravasc colloid osmotic pressure as low serum albumin
  • intravasc volume depletion
  • RAAS activation = salt and water retention

OVERFILL HYPOTHESIS

  • primary sodium retention
  • peritubular capillaries in nephron Na-K ATPase pump active so water in from lumen
  • resistance to ANP
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7
Q

What are the main 2 factors in the underfill hypothesis?

A
  • transcapillary hydrostatic pressure
    vs.
  • transcapillary oncotic pressure
    = movement of water from vasc space into interstitium
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8
Q

What is the relevance of Starling’s law?

A

underfill hypothesis

net filtration = hydrostatic - oncotic pressure

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9
Q

What is colloid oncotic pressure

A
  • driven by negative proteins in intravasc and interstitial compartments
  • draws fluid from interstitial space into capillaries
  • transcapillary oncotic pressure = difference between intravasc and interstitial COP
  • lost in nephrotic syndrome in intravasc compartment
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10
Q

Clinical presentation of nephrotic syndrome

A
  • oedema
  • bp low/normal
  • urine dip protein and maybe blood
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11
Q

Investigations for nephrotic syndrome

A
  • urine dipstix
  • PCR
  • microscopy to rule out infection
  • blood invest = FBC, clotting, U&Es, LFTs
  • specialist tests = hepatitis, HIV, Hep C, syphilis serology
  • imaging
  • US renal tract
  • renal biopsy
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12
Q

Cause of nephrotic syndrome

A

3 MAIN

  • minimal change disease
  • focal segmental glomerulosclerosis
  • membranous nephropathy
  • renal biopsy needed to determine cause
  • other less common = diabetes nephropathy, amyloid, congenital
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13
Q

Minimal change disease

A
  • children common
  • normal features on light microscopy
  • EM = fusion of podocytes
  • 90% of all NS children <10years, 50% >10 years
  • absence of microscopic haematuria
  • can be in adults
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14
Q

Focal Segmental Glomerulosclerosis

A
Focal = not all glomeruli affected
Segmental = part of glom sclerosed
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15
Q

Membranous Nephropathy Who

A
  • common in adults
  • male
  • Caucasian
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16
Q

Membranous Nephropathy Causes

A
  • thickened capillary loops
  • subepithelial immunoglobulin deposition
  • primary autoimmune
  • SLE/lupus nephritis
  • drugs = penicillamine, anti-TNF
  • malignancy
  • infection = Hep B, Hep C, HIV, malaria, syphilis
  • sarcoidosis
17
Q

Complications

A

1) infections (children)
2) thromboembolism (adults)
3) renal impairment

18
Q

Management

A
  • symptoms = oedema treatment
  • proteinuria reduce
  • dyslipidaemia statins
  • anti-coagulation
  • immunisation
  • nutrition
19
Q

How to treat oedema?

A
  • salt and water restriction!!!
  • IL fluid restriction ^
  • loop diuretics then thiazides add then aldosterone antagonists add
20
Q

How to reduce proteinuria

A
  • ACEi
  • ARBs
  • intraglomerular pressure falls
  • TREAT THE CAUSE