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Histopathology COPY > Renal pathology > Flashcards

Renal pathology Flashcards

1
Q

Renal pathology classification

A

According to part of nephron affected
Glomerulus - Nephritic, Nephrotic
Tubules + Interstitium - ATN, Tubulointerstitial, Pyelonephritis
Blood vessels - Thrombotic microangiopathy (TTP, HUS)
Whole kidney - AKI, CKD

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2
Q

Layers of glomerulus

A

Fenestrated endothelium
GBM
Podocyte foot processes (epithelial)

(Sub-epithelial = between GBM and podocytes)

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3
Q

Nephrotic syndrome

A

Damage to glomerulus = more permeable to large molecules (e.g. albumin)
1. Proteinuria (>3.5g/24h)
2. Hypoalbuminaemia
3. Oedema
4. Hyperlipidaemia
Swelling (adults peripheral, children face), frothy urine

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4
Q

3 primary causes of nephrotic syndrome

A

Minimal change
Membranous glomerular
Focal segmental

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5
Q

Most common cause of nephrotic syndrome in children

A

Minimal change disease

90% respond to steroids, 5% progress to RF

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6
Q

Childhood nephrotic syndrome
T cells destroy podocytes
EM: Loss of foot processes
90% respond to steroids, 5% develop RF

A

Minimal change disease

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7
Q 
White people
Ig deposition + complement activation destroys podocytes + GBM
Entire length of GBM 'granular'
Spike and dome GBM thickening
Poor steroid response, 40% get RF
A

Membranous glomerular

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8
Q

Black people
Ig deposition and complement activation destroys podocytes + GBM
Focal scarring of GBM (glassy hyalinolysis)
50% get RF

A

Focal segmental

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9
Q

Spike and dome GBM proliferation

A

Membranous glomerular

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10
Q

Glassy hyalinolysis

A

Focal segmental

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11
Q

Causes of membranous glomerular

A

Primary (85%) - anti-phospholipid antibodies

Secondary - AI (SLE), drugs, infections

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12
Q

Nephritic vs. nephrotic

A

Both glomerular inflammation
Nephrotic - pores let protein through
Nephritic - pores let red cells through (+ a little protein but not as much)

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13
Q

2 secondary causes of nephrotic syndrome

A

Diabetes (glucose injures - diabetic nephropathy)

Amyloidosis (amyloid deposits)

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14
Q

Mesangial matrix ‘Kimmelstiel Wilson’ nodules

Asian

A

Diabetic nephropathy

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15
Q

Congo red stain - polarised light - apple green birefringence

A

Amyloidosis

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16
Q

What are the 6 features of nephritic syndrome?

A

PHAROH

  1. Proteinuria (less than nephrotic)
  2. Haemoglobinuria (coke-coloured urine)
  3. Azootemia (raised urine and creatinine on U+Es ~RF)
  4. Red cell casts (in urine)
  5. Oliguria
  6. HTN
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17
Q

Coke coloured urine

A

Haemoglobinuria due to nephritic syndrome

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18
Q

Azootemia

A

Raised urea and creatinine

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19
Q

Red cell casts

A

Glomerulonephritis

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20
Q

What is the pathogogenesis of nephritic syndrome?

A

Damage to glomerulus
Red cells pass + a little protein pass through
Body compensates by slowing GFR (causing oliguria and HTN)
Tamm-Horsefell secreted in DCT +CD stick RBCs together to form casts

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21
Q

Protein that forms red cell casts

A

Tamm-Horsefell protein

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22
Q

What are the 5 main causes of nephritic syndrome?

A
  1. Post-strep GN
  2. IgA nephropathy + HSP
  3. Rapidly progressive GN (crescentic)
  4. Hereditary (Alport’s)
  5. Thin basement membrane disease
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23
Q

1-3w post-strep throat (/6w post impetigo)
Group A haemolytic strep
Subepithelial IgG deposition + C3 activation
- LM: Hypercellular enlarged glomerulus
- EM: IgG deposit humps
- IF: Granular starry sky appearance along entire GBM
Raised ASOT titre + C3
Usually self-limiting, 25% progress to RPGN

A

Post-strep GN

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24
Q

Prognosis post-strep GN

A

Usually self limiting

25% adults progress to RPGN

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25
Q

1-2d after URTI
Mutated IgA (I) not cleared - accumulates in mesangium - alternative complement activation
Frank haematuria
Tx: Steroids stop IgA(I) mutation. Treat HTN

A

IgA nephropathy (aka Berger’s disease)

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26
Q

Treatment IgA nephropathy

A

Steroids stop IgA(I) mutation

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27
Q

What is the difference between IgA nephropathy and HSP?

A

Both involve IgA deposition in kidney, but IgA nephropathy is kidney specific, HSP is system wide

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28
Q

What is the difference in onset of post-strep GN and IgA nephropathy?

A

Post-strep appears 1-2w after strep throat

IgA appears 1-2d after URTI

29
Q

What complement pathway is stimulated in IgA nephropathy?

A

Alternative

30
Q

Really rapid glomerular damage due to many other causes (progressive from other causes)
Oliguria + azootemia (RENAL FAILURE basically)
Very aggressive
Crescents (crescent shaped scars)
3 types - IgG, complex or Pauci immune (ANCA) mediated (all cause inflammation)

A

Rapidly progressive GN

aka Crescentic GN

31
Q

What are the three types of RPGN?

A
  1. IgG (Goodpasture’s)
  2. Complex (SLE, IgA nephropathy, post-strep)
  3. Pauci-immune (ANCA)
32
Q

Crescents
Linear IgG along GBM
Pulmonary haemorrhage

A

Goodpasture’s

33
Q

Crescents

Granular lumpy complexes along GBM

A

Complex RPGN (SLE, IgA nephropathy, post-strep)

34
Q

Crescents
Vasculitis (cANCA / pANCA)
Scanty / no deposition along GBM

A

Pauci-immune RPGN (cANCA Wegeners, pANCA MPA

35
Q

X-linked
Ineffective GBM due to alpha5 Type IV collagen mutation
Sensorineural deafness + eye problems

A

Hereditary nephritis

Aka Alport’s

36
Q

TRIAD

Nephritic syndrome + eye problems + sensorineural deafness

A

Alport’s syndrome

37
Q

AD
Diffuse GBM thinning due to alpha4 Type IV collagen mutation
Incidental microscopic haematuria
Quite common - ~5%

A

Thin basement membrane disease

aka benign familial haematuria

38
Q

Incidental microscopic haematuria

A

Thin basement membrane disease

aka benign familial haematuria

39
Q

What is the difference between Alport’s and thin basement membrane disease?

A

Alport’s is X linked, thin basement is AD

Alpha5 chain vs. alpha4 chain of type IV collagen

40
Q

Incidental microscopic haematuria

A

Thin basement membrane disease

41
Q

What are the 3 main causes of asymptomatic haematuria?

A
  1. Thin basement membrane disease
  2. IgA nephropathy ‘frank’
  3. Alport syndrome

Note that with these conditions asymptomatic haematuria is actually more common than nephritic syndrome features

42
Q

What is ATN?

A

Damage to epithelial cells of renal tubule
Dead epithelial cells are shed to form muddy brown cell casts that clog up the nephron, raising nephron pressure
Reduces pressure gradient across glomerulus starting vicious cycle of reduced renal perfusion and kidney failure
Most common renal cause of AKI

43
Q

Red cell casts

A

Nephritic syndrome

44
Q

White cell casts

A

Pyelonephritis

45
Q

Muddy brown casts

A

ATN

46
Q

What are the two main causes of ATN?

A

Ischaemia - sepsis, burns (look for RF despite recovery)

Toxins - NSAIDs, gentamicin, contrast agents, heavy metals, myoglobin, rhabdomyolysis

47
Q

Ischaemia or toxin injury
Muddy brown cell casts
Necrosis of short tubule

A

ATN

48
Q

What is tubulointerstitial nephritis?

A

Inflammation of tubule lining epithelial cells or cells of interstitium between tubules

49
Q

Renal failure days after drug exposure

Skin rash + EOSINOPHILS

A

Tubulointerstitial nephritis

50
Q

Acute vs chronic pyelonephritis

A 
Acute = inflammation resolves
Chronic = inflammation can lead to scarring; infection superimposed on obstruction (e.g. stones) / reflux
51
Q

What are the two renal thrombotic microangiopathies?

A

HUS

TTP

52
Q

What are the 3 features of thrombotic microangiopathies?

A

MAHA
Thrombocytopenia
Renal failure

53
Q

Mechanism of MAHA

A

Non-AI HA (DAAT negative)
Schistocytes
Fibrin mesh with platelet aggregation in small vessels, shears RBCs

54
Q

Child
Renal specific
Classically diarrhoea associated (0157) - child petting zoo
Renal failure most common

A

HUS

55
Q

Adult
Systemic
Not associated with diarrhoea
Neuro symptoms > renal symptoms

A

TTP

56
Q

What are the 5 main functions of the kidneys?

A

Excrete waste
Regulate fluids, electrolytes, acid/base balance
Regulate BP (renin)
Regulate RBC production (EPO)
Regulate calcium and vitamin D (1alpha-hydroxylase)

57
Q

Causes of AKI

A

Pre-renal (most common overall) - Renal hypoperfusion (burns, sepsis, RAS, acute pancreatitis)
Renal - ATN, GN, thrombotic microangiopathy
Post-renal - Obstruction (stones, tumours, BPH)

58
Q

Most common renal cause of AKI

A

ATN

59
Q

Causes of CKD

A 
Diabetes
GN
HTN + vascular disease
Chronic pyelonephritis
Polycystic kidney disease
60
Q

GFR values for kidney failure stages (1-5)

A 
Stage 1: Damage normal function >90
Stage 2: Mildly impaired 60-89
Stage 3: Moderately impaired 30-59
Stage 4: Severely impaired 15-29
Stage 5: Complete (RRT needed) <15
61
Q

Cysts + End stage renal failure

Berry aneurysms

A

Polycystic kidney disease
85% PKD1 mutation, 15% PKD2 mutation
Cysts replace renal tissue

62
Q

Polygonal cells with very clear cytoplasm
Male smoker, used to work in chemical factory
Palpable mass in flank
Haematuria
Paraneoplastic syndrome
Varicocele (compressed left renal vein)

A

(Clear cell) renal carcinoma

63
Q

Histology of RCC:

  • Clear (75%)
  • Papillary (15%)
  • Chromophobic (5%)
A
  • Polygonal cells with very clear cytoplasm
  • Dialysis pts with cysts
  • Pale eosinophilic cells
64
Q

What are the 2 main causes of RCC?

A

Mutated VHL gene on chromosome 3 (RCC has 3 letters). This may be:
SPORADIC (male, chemical exposure, smoker - solitary upper kidney tumour) or SYNDROME (VHL disease - multiple tumours + eye, CNS tumours)

65
Q

Mutated VHL gene chromosome

A

RCC

66
Q

Paraneoplastic syndromes RCC

A

EPO (polycythaemia), renin (HTN), PTHrP (hypercalcaemia), ACTH (Cushings)

67
Q

Poor prognostic factor in RCC

A

Invasion into renal vein (-> IVC spread)

68
Q

6 stages of SLE nephritis

A
  1. Minimal mesangial (deposition, no change in structure)
  2. Mesangial proliferation (deposition AND increased cellularity + inflammation)
  3. Focal (active swelling of <50% glomeruli)
  4. > 50% glomeruli
  5. Membranous (sub-epithelial deposition)
  6. Advanced sclerosing (scarring of >90%)

Histopathology COPY (19 decks)

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