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Medicine year 3 ANNA > Glomerulonephritis / Polycystic kidneys > Flashcards

Glomerulonephritis / Polycystic kidneys Flashcards

1
Q

What are the normal levels of protein in the blood?

A

Protein < 150mg/24hr

of which <30mg/24 is albumin

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2
Q

What might give you false results about proteinuria on urine dipstick?

A
  • false positive; very concentrated urine
  • false negative; very dilute urine
  • false ↓/↑ in creatinine after a protein heavy meal
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3
Q

When abnormalities occur in the glomerulus patients can present with which 5 clinical syndromes?

A
  1. Isolated haematuria /proteinuria OR haematoproteinuria
  2. Nephrotic Syndrome
  3. Acute glomerulonephritis ( acute nephritic syndrome )
  4. Rapidly progressive glomerulonephritis (RPGN )
  5. Chronic Kidney Disease including ESRD
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4
Q

How do you manage nephrotic syndrome?

A

1) . Salt restriction – Advised no salt diet
* This gives patients about 2gms of salt from the food they eat anyway, even without adding any. It is important to get a dietecian review to advice the patients on food with low salt in them.
2) . Fluid restriction to 1- 1 ½ litres over 24 hrs
3) . Diuretics
* Add diuretics to remove the peripheral odema. Over diuresis may cause pre renal Acute kidney injury, therefore monitor fluid loss by daily weights. Loss of weight should be no more than 500-750 mls a day.
4) . Add ACEI/ARB
5) . Add anticoagulation in heavy proteinuria

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5
Q

Why do we consider anti coagulation in heavily proteinuric patients?

A

Heavy proteinuria causes loss of Antithrombin 3, Protein C and S loss through the tubules. These proteins normally help blood to remain anti coagulated in the body. Loss of them makes the blood prone to clot.

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6
Q

Name 3 definite nephrotic syndromes

A
  1. Minimal Change GN
  2. Focal Segmental GN
  3. Membranous GN
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7
Q

What type of glomerulonephritis is similar to membranous GN but is a mixed nephrotic/nephritic syndrome?

A

Membranoproliferative GN

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8
Q

Name the 2 definite and 2 mixed types of nephritic syndrome

A

Definite:

  1. IgA nephropathy
  2. Rapidly Progressive / crescentic GN

Mixed:

  1. Post-infective GN
  2. Membranoproliferative GN
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9
Q

What are 2 non-glomerulonephritis causes of nephrotic syndrome?

A
  1. Diabetic nephropathy
  2. Amyloidosis
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10
Q

What are the hallmarks of nephrotic syndrome?

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

Also you will see:

  • Hyperlipidaemia
  • Lipiduria
  • Loss of antithrombin-III, proteins C and S
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11
Q

What are the hallmarks of nephritic syndrome?

A
  1. Haematuria
  2. Hypertension
  3. Oliguria (↓UO)
  4. Sediment
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12
Q

What are the characteristics of proliferative GN?

A
  • Characterised by ↑ numbers of cells in the glomerulus.
  • Usually presents with nephritic syndrome.
  • Dangerous! – can progress to end-stage-renal-failure over weeks to years e.g. rapidly progressing GN
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13
Q

Minimal change glomerulonephritis

  1. Nephrotic or nephritic?
  2. Commonly found in?
  3. Cause?
  4. Investigations?
  5. Treatments?
A
  1. Presents as nephrotic syndrome.
  2. Accounts for 80% of all nephrotic syndrome in children and 20% in adults.
  3. The cause of the disease is currently unknown
    • but some podocyte effacement
    • possibly T-cell mediated
  4. Investigations - electron microscopy reveals abnormal podocytes
  5. Treatment:
    1. Supportive care – e.g. reducing oedema
    2. Prednisolone – can halt the disease process (90% of children and 80% of adults respond well – often cured after 3 months)
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14
Q

Focal Segmental GN

  1. Nephrotic or nephritic?
  2. Commonly found in?
  3. Cause?
  4. Investigations?
  5. Treatments?
A
  1. Nephrotic
  2. Africans / Hispanics, adults and children
  3. Only some segments of some glomeruli are affected:
    1. Primary = genetic (possibly same mech as minimal change GN)
    2. Secondary: HIV, Sickle-cell, heroin abuse, kidney hyperperfusion, reflux nephropathy
  4. Specific segments of certain glomeruli develop sclerosed lesions, antibody tests are all negative.
  5. Treatment:
    1. Salt restriction and diuretics – reduce oedema
    2. Antihypertensives
    3. Statins – to treat hyperlipidaemia
    4. Cytotoxic drugs are sometimes useful.
    5. Transplant is often required – 50% progress to renal failure
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15
Q

Membranous GN

  1. Nephrotic or nephritic?
  2. Commonly found in?
  3. Cause?
  4. Investigations?
  5. Treatments?
A
  1. Nephroticc
  2. 30-50 year olds
  3. Immune complex deposition, which results in complement activation against glomerular basement membrane proteins → spikes
    1. Primary: Usually idiopathic
    2. Secondary: Hepatitis B / Malaria / Penicillamine / SLE / Ca
  4. Investigations:
    1. Microscopic analysis shows thickened glomerular basement membrane
    2. ​Immunofluorescence shows diffuse uptake of IgG.
  5. Treatment:
    • Steroids can be used if disease begins to progress
    • Prognosis follows the rule of thirds:
      • 1/3 have chronic membranous glomerulonephritis
      • 1/3 go into remission
      • 1/3 progress to end-stage renal failure
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16
Q

Membranoproliferative GN

  1. Nephrotic or nephritic?
  2. Cause?
  3. Investigations?
  4. Treatments?
A
  1. Mixed, generally nephritic
  2. Causes:
    1. Primary = immune mediated
    2. Secondary = SLE, Hepatitis
  3. Microscopy shows: Thickened basement membrane and thickened mesangium
  4. Treat the underlying cause in secondary disease.
17
Q

Post-infectious GN

  1. Nephrotic or nephritic?
  2. Commonly found in?
  3. Cause?
  4. Investigations?
  5. Treatments?
A
  1. Mixed, nephritic
  2. Post skin/throat infection
  3. Can occur after virtually any infection:
    • Tends to occur after strep pyogenes infection.
    • Typically presents 2 weeks after the infection.
  4. Proliferation of mesangial cells, Bowman space is compressed – seen as in classical crescentic glomerulonephritis (RPGN)
  5. Supportive
18
Q

IgA Nephropathy

  1. Nephrotic or nephritic?
  2. Commonly found in?
  3. Cause?
  4. Investigations?
  5. Treatments?
A
  1. Nephritic
  2. Presents in childhood as haematuria during infection of mucosal lining e.g. lung, GI, urinary tract
    • Often appears 24-48hrs after an upper respiratory tract infection.
  3. Aggregation of abormal IgA1+IgG antibodies in the mesangium → inflammation / damage
  4. A biopsy is needed to confirm the diagnosis
    • Immunohistochemistry is +ve for IgA deposits in the matrix
  5. Immunosuprression e.g. steroids
19
Q

Rapidly Progressing / crescenteric GN

  1. Nephrotic or nephritic?
  2. Commonly found in?
  3. Causes?
  4. Investigations?
  5. Treatments?
A
  1. Nephritic
  2. 50-60 year olds
  3. Any type of glomerulonephritis can progress to RPGN
    • 3 types:
      1. Type 1 - anti-GBM antibodies e.g. Goodpasture’s syndrome
      2. Type 2 - immune complexes e.g. IgA nephropathy, SLE, post-infectious GN
      3. Type 3 - ANCA (c or p)
  4. Biopsy → immunohistochemistry and antibodies
  5. High dose immunosuppression
20
Q

Name 2 Large Vessel Vasculitis types?

A
  1. Giant cell arteritis
  2. Takaysu vasculitis (aka the “pulseless disease”. Inflammation in the aorta and major branches)
21
Q

Name 2 medium vessel vasculitis types?

A
  1. Kawasaki disease
    • children present with “strawberry tongue”
    • can lead to coronary artery vasculitis
    • the leading cause of acquired heart disease in children in the U.K.
    • needs IV immunoglobulins
  2. Polyarteritis nodosa
    • associated with Hep B
    • doesn’t lead to GN
    • arteries are necrotising → GI bleed/infarct/renal arter aneurysm→rupture and bleed
22
Q

What are the 3 ANCA-associated vasculitis types?

Which type of GN are they linked to?

A
  1. GPA - granulomatoisis with polyangitis (Wegener’s granulomatosis)
  2. MPA - microscopic polyangitis
  3. EGPA - eosinophilic granulomatous polyangitis (Churg-Strauss)

All linked to RPGN!

23
Q

What are 3 characteristics of GPA?

[granulomatoisis with polyangitis (Wegener’s granulomatosis)]

A
  1. ENT involvement
  2. c-ANCA predominantly
  3. granuloma formation
24
Q

What are the 4 characteristics of EGPA?

[eosinophilic granulomatous polyangitis (Churg-Strauss)]

A
  1. p-ANCA involvement
  2. asthma
  3. eosinophilia
  4. neuropathy
25
Q

What are the phases of treatment for ANCA associated vasculitis?

A
  1. Phase 1: induce remission, 3-6 months
    • powerful cytotoxic drug
    • steroids
  2. Phase 2: maintain remission, 2 years
    • less powerful immunosuppressants
26
Q

What causes might there be of developing GN?

A
  1. Primary e.g. minimal change, FSGN
  2. Secondary:
  • Autoimmune (e.g. SLE)
  • Infections (e..g. malaria, hepatitis B & C, HIV)
  • Drugs (e.g. NSAIDs, pencilliamine)
  • Heavy metals (e.g. gold, mercury)
  • Tumours (solid tumours e.g. lung, colon and haematological malignancies e.g. multiple myeloma)
27
Q

Progression of diabetic nephropathy can result in a nephrotic syndrome, and the formation of nodules in the mesangium known as …?

A

Kimmelstiel-Wilson lesions

28
Q

How do renal cysts affect renal function?

A

Renal cysts press on:

  1. nephrons - reducing their oxygen supply, which activates RAAS and causes HTN
  2. collecting ducts - causes urinary stasis and so kidney stones
29
Q

What is the most common cause of polycystic kidney disease?

A

ADPKD = autosomal dominant polycystic kidney disease

30
Q

What other organs does ADPKD affect?

A
  • liver
  • pancreas
  • spleen
  • aortic root dissection
  • berry aneurysm (ask about FH of subarachnoid haemorrhage)
31
Q

How can ARPKD can be distinguished from ADPKD?

A
  1. by the inheritance pattern, i.e., reccessive
  2. earlier age of onset, (infancy or childhood)
  3. the obligate presence of liver disease (congenital hepatic fibrosis)
    • leads to portal HTN
      • leads to splenomegally, oesophageal varices, upper GI bleed
  4. oligohydramnios in utero
32
Q

How are renal cysts classified?

A

The Bosniak classification:

33
Q

Who gets aquired renal cysts?

A
  • Patients who have had a long duration of dialysis
  • They tend to have shrunken kidneys
  • Negative family history of cystic diseases.
34
Q

What is the diagnostic (Ravine’s) criteria for ADPKD?

A
  • Age 15-29, 3 or more cysts (unilateral or bilateral)
  • Age 30-39, 3 or more cysts (unilateral or bilateral)
  • Age 40-59, 2 or more cysts in each kidney)

Medicine year 3 ANNA (30 decks)

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