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Renal Finals KTB > Nephrotic and nephritic syndromes > Flashcards

Nephrotic and nephritic syndromes Flashcards

1
Q

Describe the aetiology of nephrotic syndrome

A

Children:
-Minimal change disease (95%)

Adults:
Primary causes:
-FSGS
-Membranous nephropathy (most common)

Secondary causes:

  • Diabetic nephropathy (common)
  • Infectious diseases: HBV, HCV, HIV
  • Inflammatory conditions eg vasculitis
  • Multiple myeloma
  • Amyloidosis
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2
Q

Define nephrotic syndrome

A

Characterised by:

1) Proteinuria (>3.5g/day)
2) Hypoalbuminaemia (<30g/L)
3) Oedema

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3
Q

Describe the presentation of nephrotic syndrome

A

May be non-specific

  • Swelling: peripheral oedema, ascites
  • Foamy urine
  • Fatigue and malaise
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4
Q

Describe the investigations for nephrotic syndrome

A
  • History and examination
  • Urine: dip, ACR (^^), 24 hour collection (rarely done)
  • Bloods: FBC, U+Es (^^), LFTs (albumin low), clotting, lipids (^^cholesterol), HbA1c, serology, antibodies, free light chains
  • USS/other imaging
  • Biopsy/ further ix
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5
Q

Describe the management of nephrotic syndrome

A
  • Treat cause!! e.g steroids/immunosuppressants (almost always need steroids)
  • ACEis/ARBs
  • Sodium +fluid restriction, diuretics (may need IV)
  • Statins
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6
Q

Describe the signs of nephrotic syndrome on examination

A

Peripheral oedema
Muehrcke’s lines (nail hypoalbuminaemia)
Xanthomas and xanthelasmata

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7
Q

Define nephritic syndrome

A

Characterised by:

1) Haematuria + mild/mod proteinuria
2) Hypertension

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8
Q

Describe the types of nephritic GN

A

Rapidly progressive GN:

1) anti-GBM disease (linear deposits)
2) Immune complex GN (granular deposits)
- Post-infectious GN
- IgA nephropathy
3) Pauci-immune- ANCA+ eg. GPA, MPA

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9
Q

Describe the presentation of IgA nephropathy

A

Presents during/shortly after acute illness eg. Strep tonsillitis
Haematuria- tea coloured urine
May have rash eg. petechiae

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10
Q

Describe the presentation of post-infectious GN

A

Presents weeks after acute illness eg strep tonsillitis
Haematuria
Fatigue

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11
Q

Describe the presentation of rapidly progressive GN

A

Haematuria
Proteinuria
Hypertension: headaches
AKI: decreased output, malaise, palpitations, swelling

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12
Q

Describe the investigations for nephritic syndrome

A
  • History and examination
  • Urine: dip, ACR/PCR, 24 hour collection (rare)
  • Bloods: FBC, CRP/ESR, U+Es, LFTs, lipids, antibodies, serology
  • USS
  • CXR in RPGN (pulmonary haemorrhage), CTCAP for malignancy
  • Renal biopsy
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13
Q

Describe the management of nephritic syndrome

A

Depends on cause

  • Mild (IgA nephropathy, post-infectious): conservative
  • Mod/severe: ACEis, steroids/immunosuppressants
  • RPGN: admit, AKI management, steroids/immunosuppressants, consider plasmapharesis
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14
Q

What are the hallmarks of glomerular damage?

A

Proteinuria (specifically podocyte damage)

Haematuria w/ red cell casts

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15
Q

Describe the aetiology of PKD

A

Mostly autosomal dominant inherited condition

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16
Q

Describe the presentation of PKD

A 
May be detected incidentally eg. USS in pregnancy
Abdominal/flank pain 
Haematuria
Abdo mass; early satiety etc 
Headaches
Recurrent UTIs: common
17
Q

Describe the investigations for PKD

A
  • History and examination
  • BP measurement
  • Urinalysis, 24 hour biochemistry (if stones)
  • Bloods: FBC, U+Es, lipids, HbA1c (RF management)
  • USS!! -> CT/MRI

Extrarenal manifestations:

  • ECG and echo
  • CTH (aneurysms)
18
Q

Describe the pathophysiology of PKD

A

Cysts forming in kidneys -> compression of normal tissues, fibrosis -> progressive renal impairment
+ cysts in liver, berry aneurysms

19
Q

Describe the signs of PKD on examination

A

HTN
Hernias
Palpable abdominal mass/ballot-able kidneys
Hepatomegaly

20
Q

Describe the management of PKD

A

Conservative:

  • Lifestyle: renoprotective diet
  • Avoid oestrogens (liver cysts)

Medical:

  • Tolvaptan (slows cyst development)
  • Hypertension Mx: ACEi/ARB 1st line
  • Reduce CV RFs: statin, glycaemic control
  • RRT

Surgical:
-Transplant

21
Q

Describe the pathophysiology of renal artery stenosis

A

Narrowing of the renal arteries -> reduced renal blood flow
-> activation of the renin-angiotensin system
-> increase sodium + water resorption -> increase BP
+ remodelling of nephron

22
Q

Describe the aetiology of renal artery stenosis

A 
Atherosclerosis (90%): M >F, vasculopaths
Fibromuscular dysplasia (10%): young F
23
Q

Describe the presentation of renal artery stenosis

A
  • Refractory hypertension
  • Accelerated/malignant HTN
  • Acute deterioration in renal function
  • Flash pulmonary oedema
24
Q

Describe the investigations for renal artery stenosis

A
  • History and examination
  • BP
  • Urinalysis
  • Bloods: FBC, U+Es, lipids, HbA1c (RF screen), aldosterone:renin ratio (normal/low)
  • Duplex USS -> CTA/MRA

Screen for end-organ damage:

  • ECG
  • Fundoscopy
25
Q

Describe the management of renal artery stenosis

A

Conservative:

  • Avoid nephrotoxics
  • Renoprotective lifestyle measures eg. smoking cessation, weight loss, exercise

Medical:

  • Manage RF: statin, glycaemic control, aspirin
  • ACEi/ARB (but monitor very closely) or thiazides/loops

Surgical/interventional:

  • Vascular intervention eg. stenting (2nd line)
  • Surgical reconstruction

Renal Finals KTB (2 decks)

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