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YEAR 5: Histopathology > Histo: Renal Disease > Flashcards

Histo: Renal Disease Flashcards

1
Q

List the major functions of the kidneys.

A
  • Excretion of metabolic waste products and foreign chemicals
  • Regulation of fluid, electrolytes and acid/base balance
  • Regulation of blood pressure (renin)
  • Regulation of calcium and bone metabolism (1,25-dihydroxy vitamin D)
  • Regulation of haematocrit (EPO)
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2
Q

List some key anatomical features of the kidneys.

A
  • Retroperitoneal
  • T12-L3
  • Right kidney lies lower
  • Mean length = 11cm
  • Normal weight = 115-170g
  • 1 million nephrons per kidneys
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3
Q

What proportion of cardiac output goes to the kidneys?

A

20%

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4
Q

By what mechanism is blood filtered through the glomerulus?

A
  • High hydrostatic pressure (60 mmHg)
  • Podocytes create a charge-dependent (anionic) and size-dependent barrier
  • Filtration rate = 125 ml/min
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5
Q

Describe the role of the following parts of the nephron:

  1. Proximal convoluted tubule
  2. Loop of Henle
  3. Distal convoluted tubule
  4. Collecting duct
A
  1. Proximal convoluted tubule
    • Actively absorbs sodium
    • Carries out hydrogen exchange to allow carbonate resoprtion
    • Co-transport of amino acids, phosphate and glucose
    • Reabsorption of potassium
  2. Loop of Henle
    • Descending limb and thin ascending limb: permeable to water, impermeable to ions and urea
    • Ascending limb: actively resorbs sodium and chloride
    • This creates a counter-current multiplier that is aligned with the vasa recta
  3. Distal convoluted tubule
    • Impermeable to water
    • Regulates pH by active transport of protons and bicarbonate
    • Regulates sodium and potassium by active transport (aldosterone)
    • Regulates calcium (PTH, 1,25-dihydroxy vit D)
  4. Collecting duct
    • Reabsorb water (principal cells, ADH)
    • Regulates pH (intercalated cells, proton excretion)
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6
Q

Describe how immune complex deposition can lead to renal disease.

A

Complex deposition in the glomerulus results in complement and inflammatory cell activation resulting in damage to the kidney

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7
Q

List some signs and symptoms of renal disease.

A
  • Haematuria
  • Proteinuria
  • Uraemia
  • Hypertension
  • Oliguria/anuria
  • Polyuria
  • Oedema
  • Colic
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8
Q

List some genitourinary malformations of the kidney.

A
  • Agenesis
  • Renal fusion
  • Ectopic kidney
  • Renal dysplasia
  • PUJ obstruction
  • Posterior urethral valve
  • Vesicoureteric reflux
  • Ureteral duplication
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9
Q

Outline the presentation of polycystic kidney disease.

A
  • Hypertension
  • Haematuria
  • Flank pain
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10
Q

What is the inheritance pattern of polycystic kidney disease and which genes are implicated?

A

Autosomal dominant (most of the time)

Genes: PKD1 and PKD2

NOTE: PKD is associated with an increased risk of berry aneurysms (and subarachnoid haemorrhage)

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11
Q

In which group of renal patients do renal cysts often develop?

A

Patients with end-stage renal disease who are on dialysis

Cysts are often multiple, bilateral and cortical and medullary

NOTE: cystic disease is associated with increased risk of malignancy (papillary renal cell carcinoma)

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12
Q

List some causes of acute renal failure.

A
  • Pre-renal = failure of perfusion (shock, heart failure)
  • Renal = ATN, acute glomerulonephritis, thrombotic microangiopathy
  • Post-renal = obstruction
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13
Q

What is the most common cause of acute renal failure?

A

Acute tubular injury

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14
Q

List some causes of acute tubular injury.

A

Ischaemia

Toxins (contrast, haemoglobin, myoglobin, ethylene glycol)

Drugs

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15
Q

Which commonly used class of drugs predisposes to acute tubular injury?

A

NSAIDs - inhibits vasodilatory prostaglandins which predisposes to ATN

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16
Q

How does acute tubular injury lead to reduced GFR?

A
  • Blockage of tubules by casts
  • Leakage from tubules into interstitial space
  • Secondary haemodynamic changes
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17
Q

What is acute tubulo-interstitial nephritis?

A

Immune injury to tubules and interstitium

Can be caused by infection and drugs (NSAIDs, antibiotics, diuretics, allopurinol, PPIs)

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18
Q

Describe the histological appearance of acute tubulo-interstital nephritis.

A

Heavy interstitial infiltration with eosinophil and granulomas

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19
Q

What causes crescents to appear in acute glomerulonephritis?

A

Occurs in severe glomerulonephritis due to proliferation of cells within Bowman’s capsule

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20
Q

List some causes of acute crescentic glomerulonephritis.

A
  • Immune complex deposition
  • Anti-GBM disease (Goodpasture’s)
  • Pauci-immune (ANCA)

NOTE: these can rapidly lead to irreversible renal failure

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21
Q

List some causes of immune complex-associated crescentic glomerulonephritis.

A
  • SLE
  • IgA nephropathy
  • Post-infectious glomerulonephritis
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22
Q

What techniques can be used to visualise immune complexes in these diseases?

A

Immunohistochemistry

Electron microscopy

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23
Q

What are the antibodies directed against in anti-GBM disease?

A

Against the C-terminal domain of type IV collagen

NOTE: these antibodies can cross-react with the alveolar basement membrane leading to pulmonary haemorrhage and haemoptysis

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24
Q

Describe the immunohistochemistry picture produced in anti-GBM disease,

A

Linear deposition of IgG on the glomerular basement membrane

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25
Q

What are the main features of pauci-immune crescentic glomerulonephritis?

A
  • Scanty glomerular immunoglobulin depositis
  • Usually associated with ANCA
  • Triggers neutrophil activation and glomerular necrosis
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26
Q

What is thrombotic microangiopathy?

A
  • Damage to the endothelium in glomeruli, arteriols and arteries resulting in thrombosis
  • Red cells can be damaged by fibrin causing MAHA or HUS
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27
Q

List some causes of thrombotic microangiopathy.

A
  • Diarrhoea-associated: E. coli - toxins can target the renal epithelium
  • Non-diarrhoea associated: defects in complement regulation, deficiency of ADAMTS13, drugs, radiation, hypertension, scleroderma, antiphospholipid syndrome
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28
Q

What are the characteristic features of nephrotic syndrome?

A
  • Proteinuria (>3,5 g/day or >300mg/mmol PCR)
  • Hypoalbuminaemia
  • Oedema
  • Hyperlipidaemia
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29
Q

List some causes of nephrotic syndrome.

A
  • Primary glomerular disease (non-immune complex mediated)
    • Minimal change disease
    • Focal segmental glomerulosclerosis
  • Primary renal disease (immune complex mediated)
    • Membranous glomerulonephritis
  • Systemic disease
    • SLE
    • Amyloidosis
    • Diabetes mellitus
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30
Q

What is minimal change disease?

A
  • most common cause of nephrotic syndrome in children
  • Glomeruli look normal on light microscopy, but electron microscopy shows loss of foot processes
  • Generally responds well to steroids and immunosuppression
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31
Q

Describe the histological appearance of focal segmental glomerulosclerosis.

A

Some glomeruli are partially scarred

NOTE: this responds less well to immunosuppression

32
Q

What is membranous glomerulonephritis?

A
  • Common cause of nephrotic syndrome in adults
  • Characterised by diffuse glomerular basement membrane thickening and immune complex deposition along the entire GBM
  • Primary disease is autoimmune
  • It can occur secondary to epithelial malignancy, SLE, drugs and infections
33
Q

Which antibodies are often found in primary membranous glomerulonephritis?

A

Antibodies against phospholipase A2 type M receptor (PLA2R)

34
Q

Describe the typical progression of diabetic nephropathy.

A

Typically begins with microalbuminuria

Progresses to proteinuria and, eventually, nephrotic syndrome

35
Q

List and describe the stages of diabetic nephropathy.

A
  • Stage 1: thickening of the basement membrane on electron microscopy
  • Stage 2: increase in mesangial matrix, without noduls
  • Stage 3: nodular lesions/Kimmelstein-Wilson nodules
  • Stage 4: advanced glomerulosclerosis
36
Q

What is amyloidosis?

A

Deposition of extracellular proteinaceous material exhibiting beta-pleated sheet structure

37
Q

What are the two types of amyloidosis?

A
  • AA - derived from serum amyloid protein and associated with chronic inflammatory disease
  • AL - derived from immunoglobulin light chains usually as a result of multiple myeloma
38
Q

Name two causes of isolated microscopy haematuria.

A
  • Thin basement membrane
  • IgA nephropathy
39
Q

How can the cause of asymptomatic proteinuria be confirmed?

A

Renal biopsy (could be caused by several abnormalities)

40
Q

What is thin basement membrane disease and what causes it?

A
  • Basement membrane <250 nm thickness
  • Caused by a hereditary defect in type IV collagen synthesis
  • Microscopic haematuria is the only consequence in most cases
41
Q

What is Alport syndrome?

A
  • X-linked disease caused by a mutation in the alpha-5 subunit of type IV collagen (some forms affect alpha-3 and alpha-4)
  • Leads to progressive damage resulting in renal failure in middle-age
  • Often accompanied by deafness and ocular disease
42
Q

What is IgA nephropathy?

A
  • Most common cause of glomerulonephritis
  • Caused by mesangial IgA immune complex deposition
  • 30% will progress to end-stage renal failure

NOTE: Henoch-Schonlein purpura is a type of IgA nephropathy

43
Q

List some causes of chronic kidney disease and state which is most common.

A
  • Diabetes mellitus
  • Glomerulonephritis
  • Polycystic kidney disease
  • Pyelonephritis
  • Hypertension
  • Renal vascular disease
44
Q

What are some diseases associated with chronic kidney disease?

A
  • Ischaemic heart disease
  • Calcium and phosphate derangement (due to resulting hyperparathyroidism, osteomalacia and osteoporosis)
45
Q

What are consequences of hypertensive nephropathy?

A
  • Shrunken kidneys with granular cortices
  • Nephrosclerosis on histology (arterial hyalinosis, arterial intimal thickening, ischaemic glomerular changes, segmental and global glomerulosclerosis)
46
Q

What system is used to classify lupus nephritis?

A

ISI/RPS classification

47
Q

What histological feature is suggestive of diabetic nephropathy?

A

Kimmelstein-Wilson nodules

48
Q

What is another name for Alport’s syndrome?

A

Hereditary nephritis

49
Q

How do each of the primary causes of nephrotic syndrome respond to steroids?

A

MCD - well, 90% respond
FSGS - 50% respond
MN - poorly

50
Q

What conditions are associated with MCD?

A

Asthma and eczema - may have an allergic component (e.g. sometimes triggered by recent allergic reaction)

51
Q

What is the management of MCD?

A

1st line - steroids
2nd line - cyclosporin

52
Q

What is the management of FSGS?

A

1st line - steroids
2nd line - calcineurinin inhibitors (e.g. tacrolimus)

53
Q

Which ethnicity is diabetic nephropathy particularly associated with?

A

Asians

54
Q

What are the symptoms of nephritic syndrome?

A

PHAROH

Proteinuria - less significant than nephrotic syndrome
Haematuria
Azootemia - high creatinine and urea
Red cell casts
Oliguria
Hypertension

55
Q

What are the main causes of nephritic syndrome?

A
  • Acute post-infectious (post-Strep) glomerulonephritis
  • IgA nephropathy (Berger’s disease)
  • Rapidly progressive crescentic glomerulonephritis
56
Q

What is typically the cause of post-infectious glomerulonephritis?

A

Lancefield Group A b-haemolytic Streptococcus (e.g. strep progenes) infection

Such as impetigo or strep throat

57
Q

What changes in blood tests would be seen in post-infectious glomerulonephritis?

A

Elevated ASOT (anti-streptolysin) titres
Reduced C3

58
Q

What changes on histology (light/fluoro/electron) would be seen in post-infectious glomerulonephritis?

A

Light - cellularity of glomeruli increased
Fluorescence - IgG and C3 deposits in GBM
Electron - subendothelial humps

59
Q

What is the most common cause of glomerulonephritis worldwide?

A

IgA nephropathy

60
Q

What is the classical presentation of IgA nephropathy?

A
  • Presents 1-2 days after an URTI with frank haematuria
  • May be associated with vasculitis rash
  • Can progress to ESRF

Can be differentiated from post-infectious GN as it occurs quicker (days rather than weeks)

61
Q

What changes in blood tests would be seen in IgA nephropathy?

A

Raised IgA levels

62
Q

What changes on histology would be seen in IgA nephropathy?

A

IgA and C3 deposits in mesangium

63
Q

How can crescentic GN be differentiated from other causes of nephritic syndrome?

A

Oliguria and renal failure will often be more pronounced

64
Q

What are some examples of Pauci-immune crescenteric GN?

A
  • Wegner’s granulomatosis (c-ANCA)
  • Microscopic polyangitis (p-ANCA)
65
Q

What is acute interstitial nephritis?

A

Typically a hypersensitivity reaction, usually to a drug (NSAID, Abx, diuretics) that begins days after exposure to the drug

66
Q

When is chronic interstitial nephritis seen?

A

Usually in elderly patients with chronic analgesic use (NSAIDs/paracetamol) with symptoms occurring late in disease

67
Q

What is the triad of HUS?

A
  • Thrombocytopenia
  • MAHA
  • Renal failure
68
Q

What is the pentad of TTP?

A
  • Thrombocytopenia
  • MAHA
  • Renal failure
  • Neurological symptoms - seizures, confusion
  • Fever
69
Q

Why does TTP result in neurological symptoms?

A

Thrombi are not just confined to the kidneys (as in HUS) and instead can circulate, including the CNS

70
Q

What blood test results would be expected in HUS/TTP?

A
  • Low Hb
  • Low platelets
  • Signs of haemolytic - high bilirubin, LDH, reticulocytes
  • Schistocytes on blood film (fragmented RBCs suggestive of MAHA)
  • Negative Coomb’s test
71
Q

What chromosome are the PKD mutations on respectively?

A

PKD1 = chromosome 16
PKD2 = chromosome 4

72
Q

What are the clinical features of PKD?

A

MISHAPES

Mass (abdominal)
Infected cysts and Increased BP
Stones
Haematuria
Aneursyms (berry)
Polyuria and nocturia
Extra-renal cysts
Systolic murmur

73
Q

Why might there be a systolic murmur in patients with PKD?

A

Mitral valve prolapse

74
Q

Where can cysts occur outside of the kidneys in PKD?

A

Ovaries
Liver
Pancreas
Seminal vesicles

75
Q

What are some paraneoplastic syndromes associated with renal cell carcinoma?

A

Polycythaemia (increased EPO)
Hypercalcaemia
HTN
Cushing’s syndrome
Amyloidosis

YEAR 5: Histopathology (20 decks)

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