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YR5 Histopathology > Crash course: Renal > Flashcards

Crash course: Renal Flashcards

1
Q

What is AKI? What is it measured by?

A

acute decline in renal function, leading to fall in urine output

Measured by rise in creatinine + urea

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2
Q

What is CKD? How is it measured?

A

Decline in renal function due to progressive damage present for >3 months

Measured via decline in eGFR

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3
Q

What are the stages of CKD based on eGFR?

A

1: >90
2: 60-89
3a: 45-59
3b: 30-44
4: 15-29
5: <15 = end stage, dialysis

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4
Q

What are the caveats of stage 1 and 2 CKD grades?

A

If stage 1/2 based on eGFR but NO Sx, NOT CKD

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5
Q

What are the 2 most common causes of CKD?

A

Diabetes
HTN

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6
Q

Give 2 less common causes of CKD

A

Autosomal dominant polycystic kidney disease

Untreated AKI (Pyelonephritis, ATN, obstruction)

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7
Q

What are the 3 broad causes of AKI?

A

PRE-renal: decrease in flow to the kidneys.

RENAL: direct damage to nephrons

POST-renal: ‘Surgical causes”- physical outflow obstruction

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8
Q

From most to least common, what are the broad causes of AKI

A

Pre-renal
Post-renal
Renal

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9
Q

Give 5 causes of pre-renal AKI

A

Hypovolaemia
Sepsis
CCF
Renal artery stenosis
ACE inhibitors

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10
Q

Give 6 causes of renal AKI

A

Ischaemia
Nephrotoxins
Glomerulonephritis
Interstitial nephritis
Hepatorenal syndrome
HUS / TTP

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11
Q

Give 4 causes of post-renal AKI

A

Stone
Tumour
Prostate
Blocked catheter

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12
Q

Which 3 structures can be damaged to result in renal causes of AKI?

A

Glomerulus: Nephrotic + Nephritic syndrome

Blood vessels: HUS + TTP

Tubules: ATN + acute interstitial nephritis

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13
Q

Give 4 causes of nephrotic syndrome

A

Minimal change
Membranous
FSGS
Secondary causes

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14
Q

What triad characterises Nephrotic syndrome?

A

Peripheral oedema

Proteinuria (3g/day or PCR >300mg)

Low serum albumin

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15
Q

Give 2 other features of nephrotic syndrome

A

Increased cholesterol

Increased clotting tendency- Antithrombin III is lost

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16
Q

What is the pathophysiology in all causes of nephrotic syndrome?

A

Breakdown of PODOCYTES (filtration barrier)

Large molecules e.g. Protein not filtered out - lost in urine

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17
Q

What is the broad management of nephrotic syndrome?

A

Steroids

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18
Q

What is the most common cause of nephrotic syndrome in kids?

A

Minimal change disease

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19
Q

What is seen on histology in minimal change disease?

A

Light microscopy: Nothing

Electron microscopy: Loss of podocyte foot processes

Immunofluorescence: Nothing

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20
Q

What is the prognosis for minimal change disease?

A

Majority respond to Prednisolone ~(90%)

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21
Q

In which population is membranous glomerulonephropathy seen?

A

Adults

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22
Q

What do immunofluorescence microscopes detect?

A

Immune complexes

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23
Q

What is seen on histology in membranous glomerulonephropathy?

A

Light microscopy: Diffuse basement membrane thickening

Electron microscopy: Spikey immune complex deposits

Immunofluorescence: Immune complexes across all of basement membrane

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24
Q

How does membranous glomerulonephropathy respond to steroids?

A

Poor response

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25
Q

Give 2 associations to Membranous glomerulonephropathy

A

SLE
Anti-phospholipase A2 antibodies

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26
Q

What is focal segmental glomerulonephritis? (FSGS)

A

Focal = Only some glomeruli are damaged (vs diffuse)

Segmental = Only some regions of each individual glomerulus damaged

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27
Q

Which population is affected by focal segmental glomerulonephritis?

A

Adults

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28
Q

What is seen on histology in Focal segmental glomerulonephritis?

A

Light microscopy: Focal + segmental scarring

Electron microscopy: Loss of foot processes

Immunofluorescence: Nothing

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29
Q

How does focal segmental glomerulonephritis respond to steroids?

A

Not great (better than membranous glomerulonephropathy)

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30
Q

Give 2 secondary causes of nephrotic syndrome. What is seen on histology?

A

Diabetes: Kimmelstiel Wilson nodules

Amyloidosis: apple green birefringence on Congo red stain

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31
Q

What are the 2 types of amyloidosis? What causes each?

A

AA: chronic inflammation (e.g RA, SLE)

AL: Light chains (MM): plasma cells produce Abs, Abs clog up kidneys + cause damage

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32
Q

Give 5 causes of nephritic syndrome

A

IgA
Post streptococcal
Rapidly progressive (crescentic)
Alport’s syndrome (hereditary)
Benign familial

33
Q

What triad characterises nephritic syndrome?

A

HTN
Haematuria
Peripheral oedema

34
Q

What is seen in the urine in nephritic syndrome?

A

Red cell casts- “Cola-coloured”

35
Q

What is seen on bloods in nephritic syndrome?

A

Deranged U+Es

36
Q

What is the pathophysiology of nephritic syndrome?

A

Big proteins + complexes damage delicate blood vessels + cause inflammation

37
Q

Give 3 features of IgA nephropathy?

A

Commonest cause of nephritic syndrome worldwide

After group A Streptococcal infection (1-2 days remember: IgA = Acute)

Deposition of IgA immune complexes within glomeruli

38
Q

What is seen on immunofluorescence in IgA nephropathy?

A

IgA immune deposits in mesangium

39
Q

What is the prognosis for IgA nephropathy?

A

1/3 get better
1/3 get CKD
1/3 need dialysis

40
Q

Give 2 features of post-streptococcal glomerulonephritis

A

After group A strep infection (1-3w)

Thought to be due to antigen mimicry + immune complex deposition

41
Q

What is seen on bloods in post-streptococcal glomerulonephritis?

A

Raised Anti-streptolysin-O titre
Reduced C3 (as immune complex mediated)

42
Q

What is seen on immunofluorescence in post-streptococcal glomerulonephritis?

A

Granular IgG deposits in basement membrane

43
Q

What is management in post-streptococcal glomerulonephritis?

A

Supportive

44
Q

What is Rapid progressive nephritic syndrome? (crescentic)

A

Most aggressive type of glomerulonephritis causing renal failure in weeks.

Characterised by severity + presence of crescents (macrophages in Bowman’s space)

45
Q

Name 3 causes of rapidly progressive nephritic syndrome

A

Goodpasture’s
Immune complex mediated
Pauci-immune (ANCA associated)

46
Q

What is Goodpasture’s characterised by?

A

Presence of Anti-glomerular basement membrane antibodies
Causes glomerulonephritis + pulmonary haemorrhages

47
Q

What is the antigen targeted in goodpastures disease?

A

Alpha-3 subunit of type IV collagen found in the basement membrane of the lungs + kidneys.

48
Q

What is seen on histology in Goodpasture’s?

A

Light microscopy: Crescents

Immunofluorescence: LINEAR deposition of IgG in GBM

49
Q

Give 4 causes of immune complex mediated rapidly progressive nephritic syndrome

A

SLE
IgA nephropathy
Post-infectious
HSP

50
Q

Describe histology in immune complex mediated rapidly progressive nephritic syndrome

A

Light microscopy: Crescents
Immunofluorescence: BUMPY deposition of immune complexes in GBM or mesangium

51
Q

What are the subtypes of Pauci-immune rapidly progressive nephritic syndrome?

A

cANCA: granulomatosis with polyangiitis (GPA)

pANCA: microscopic polyangitis (MPA), eosinophilic granulomatosis with polyangiitis (eGPA)

52
Q

What is seen on histology in Pauci-immune rapidly progressive nephritic syndrome?

A

Light microscopy: Crescents
Immunofluorescence: No/ scanty immune complexes

53
Q

What other features may be seen in Pauci-immune rapidly progressive nephritic syndrome?

A

Vasculitis: Skin rash, pulmonary haemorrhage

54
Q

What causes Alport’s syndrome?

A

X-linked abnormalities in type IV collagen

55
Q

What triad is seen in Alport’s syndrome?

A

Nephritic syndrome
Bilateral sensorineural deafness
Lens dislocation

56
Q

What is the prognosis of Alport’s syndrome?

A

Progressive, causes end stage renal failure in early adulthood

57
Q

What causes benign familial haematuria?

A

Autosomal dominant abnormality in type IV collagen
aka. thin basement membrane disease

58
Q

What are the symptoms of benign familial haematuria?

A

Asymptomatic haematuria
No other issues generally

59
Q

What is the most common renal cause of AKI?

A

Acute tubular necrosis

60
Q

What is acute tubular necrosis?

A

Damage to tubules
Tubule cells die + shed leading to presence of brown casts in urine

61
Q

Give 2 causes of acute tubular necrosis

A

Hypovolaemia

Toxins:
* Aminoglycoside abx: gentamicin
* Myoglobin (rhabdomyolysis)
* IV contrast

62
Q

What should you think of in acute interstitial nephritis? What occurs?

A

Think of allergic reaction to medications

Interstitial infiltrate + eosinophils excreted as white cell casts or white cells in urine with no infection (sterile pyuria)

+/- rash
+/- fever

63
Q

Give 3 drugs that may precipitate acute interstitial nephritis?

A

Penicillins
Allopurinol
NSAIDs

64
Q

What causes chronic interstitial nephritis?

A

Long term paracetamol/ NSAID use

65
Q

What is haemolytic uraemia syndrome?

A

Microangiopathy characterised by:
* Progressive renal failure (AKI)
* Microangiopathic haemolytic anaemia (MAHA)
* Thrombocytopenia

66
Q

What is the most common cause of HUS?

A

E. coli O157:H7

(shiga toxin-producing E. coli or STEC)

67
Q

Describe the pathophysiology of HUS

A
  1. Gastroenteritis (E.coli 90%) → toxin
  2. Endothelial damage
  3. Thrombosis, platelet consumption + fibrin strand deposition → ↓ Platelets
  4. Destruction of RBCs: schistocytes, ↓ Hb
68
Q

Where are micro thrombi in HUS?

A

Microthrombi confined to kidneys

69
Q

What pentad of features characterises Thrombotic thrombocytopenic purpura?

A

Haemolytic anaemia
Uraemia
Thrombocytopenia
Fever
Neurological Sx: seizures, hemiparesis, impaired consciousness, impaired vision

70
Q

What is the mortality in TTP if untreated?

A

90%

71
Q

Give 6 causes of TTP

A

Post-infection e.g. UTI, GI
Pregnancy
Drugs: ciclosporin, OCP, penicillin, clopidogrel, aciclovir
Tumours
SLE
HIV

72
Q

What is the pathophysiology of TTP?

A
  1. Deficiency in protease ADAMTS13 that cleaves vWF
  2. Large vWF multimers form
  3. Platelet aggregation + fibrin deposition
  4. Microthrombi
73
Q

Where do microthrombi occur in TTP?

A

Everywhere, esp. CNS

74
Q

What is the aetiology of polycystic kidney disease? What does this cause?

A

Autosomal Dominant
Due to mutation in PKD gene encoding polycystin

Causes haematuria + kidney failure

75
Q

Give 2 extra renal manifestations of PKD

A

Liver cysts (common)
Berry aneurysms (leading to SAH)

76
Q

What is the aetiology of lupus nephritis? What is seen?

A

Damage due to immune complex deposition,
See wire loop capillaries + lumpy immune complex deposition

77
Q

What are the 2 extremes of lupus nephritis?

A

Early stage (stage 1): only mesangial disease- not affecting kidney function

Advanced (stage 6): >90% sclerosis = end stage

78
Q

A 25M is involved in an RTA. On arrival his BP is 65/40 mmHg but he is quickly resuscitated and stabilised in ITU.
2 days later the SHO notices that over the past 6h, his catheter urine output has only been 50ml. What is the cause of his renal dysfunction?

A

Acute tubular necrosis

Often get a pre-renal AKI, rehydrate them, become stable, but then renal function continues to decline- because you cant reverse necrosis
(he has progressed from pre-renal to ATN)

YR5 Histopathology (27 decks)

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