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YEAR 5: Histopathology PM (COPY) > 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
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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
proximal convoluted tubule.

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
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6
Q

Describe the role of the loop of Henle.

A

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
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7
Q

Describe the role of the distal convoluted tubule.

A

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)
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8
Q

Describe the role of the collecting duct.

A

Collecting duct

  • Reabsorb water (principal cells, ADH)
  • Regulates pH (intercalated cells, proton excretion)
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9
Q

Describe how disease of the kidney can be classified according to the part of the nephron it affects

A

1. Glomerulus

Nephrotic:

  • Primary = MCD, FSGS, MGD
  • Secondary = diabetes, amyloidosis, SLE

Nephritic:

  • Acute post-infectious (post-streptococcal)
  • IgA nephropathy (Berger Disease)
  • Rapidly progressive glomerulonephritis
  • Alport’s syndrome (hereditary nephritis)
  • Thin basement membrane disease (Benign familial haematuria)

2. Tubules & interstitium

  • Acute tubular necrosis
  • Tubulointerstitial nephritis

3. Blood vessels

  • Thrombotic microangiopathies (HUS, TTP)
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10
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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11
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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12
Q

Outline the presentation of polycystic kidney disease.

A
  • Hypertension
  • Haematuria
  • Flank pain

Adult onset

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13
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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14
Q

In which group of renal patients do renal cysts often develop?
What do they increase the risk of?

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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15
Q

What is Alport syndrome?

A

Genetic condition affecting type IV collagen. Leads to triad of:

  • Kidney disease
  • Hearing loss
  • Eye changes (lenticonus, cataracts)
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16
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 to urine flow
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17
Q

What is the most common cause of acute renal failure?

A

Reduced renal perfusion

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18
Q

List some causes of acute tubular injury.

A
  • Ischaemia
  • Toxins - contrast, haemoglobin, myoglobin, ethylene glycol, drugs)
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19
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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20
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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21
Q

Describe the histological appearance of ATN

A

Necrosis of short segments of tubules

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22
Q

What is acute tubulo-interstitial nephritis?

A

Inflammation of the renal interstitium, typically due to immune-mediated hypersensitivity reaction

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

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23
Q

Describe the histological appearance of acute tubulo-interstital nephritis.

A

Heavy interstitial infiltration with eosinophil and granulomas

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24
Q

What are some key signs of acute glomerulonephritis?

A
  • Oligo/anuria
  • Haematuria
  • Erythrocyte and leukocyte casts on MCS
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25
Q

What is rapidly progressive (crescentic) GN?

A

Most aggressive form of GN – can cause ESRF within weeks.

Presents as a nephritic syndrome, but oliguria and renal failure are more pronounced

26
Q

What causes crescents to appear in acute glomerulonephritis?

A

Occurs in severe glomerulonephritis due to proliferation of macrophages & parietal cells in Bowman’s space which pushes glomerulus to one side

27
Q

Describe the classification of acute crescentic glomerulonephritis.

A

Classification based on immunological findings:

  • Type 1. Anti-GBM antibody (Goodpasture’s)
  • Type 2. Immune complex mediated (SLE)
  • Type 3. Pauci-immune (ANCA-associated - GPA)

NOTE: these can rapidly lead to irreversible renal failure

28
Q

List some causes of immune complex-associated (type 2) crescentic glomerulonephritis.

A
  • SLE
  • IgA nephropathy
  • Post-infectious glomerulonephritis
  • HSP
29
Q

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

A
  • Immunohistochemistry (fluorescence microscopy)
  • Electron (light) microscopy
30
Q

How does immune complex-associated crescentic GN appear on fluorescence microscopy?

A

Granular (lumpy bumpy) IgG immune complex deposition on GBM/mesangium

31
Q

What are the antibodies directed against in anti-GBM disease?
How can these antibodies be detected?

A
  • Against the C-terminal domain of type IV collagen (COL4-A3)
  • Detected by serology

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

32
Q

Describe the immunohistochemistry picture produced in anti-GBM disease

A

Linear deposition of IgG on the glomerular basement membrane

33
Q

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

A
  • Lack of / scanty glomerular immunoglobulin depositis
  • Usually associated with ANCA
  • Triggers neutrophil activation and glomerular necrosis
  • Vasculitis (elsewhere) – particularly presenting as skin rashes or pulmonary haemorrhage
34
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
35
Q

List some types of thrombotic microangiopathy.

A

HUS: Thrombi confined to kidneys

  • Typical HUS - usually associated with diarrhoea caused by E.coli O157:H7 (outbreaks caused by children visiting petting zoos/eating undercooked meat)
  • Atypical HUS (non-diarrhoea associated) - due to abnormal proteins in complement pathway/endothelium (can be familial)
  • Triad - thrombocytopaenia, MAHA, renal damage

TTP: Thrombi occur throughout circulation, esp. in CNS

  • A genetic / acquired deficiency of ADAMTS13
  • Pentad - thrombocytopaenia, MAHA, renal damage, CNS abnormalities, fever

Also:

  • Drugs, radiation, hypertension, scleroderma, antiphospholipid syndrome
36
Q

What are the characteristic features of nephrotic syndrome?

A
  • Proteinuria (>3.5 g/day or >300mg/mmol PCR)
  • Hypoalbuminaemia
  • Oedema
  • Hyperlipidaemia
37
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
38
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
39
Q

Describe the histological appearance of focal segmental glomerulosclerosis.

A

Focal and segmental glomerular consolidation and scarring
Hyalinosis

NOTE: this responds less well to immunosuppression

40
Q

What is membranous glomerulonephritis?

A
  • Common cause of nephrotic syndrome in adults
  • Characterised by immune deposits outside the glomerular basement membrane (subepithelial - ‘spikey’)
  • Primary disease is autoimmune
  • It can occur secondary to epithelial malignancy, SLE, drugs and infections
41
Q

Which antibodies are often found in primary membranous glomerulonephritis?

A

Antibodies against phospholipase A2 type M receptor (PLA2R)

42
Q

Describe the typical progression of diabetic nephropathy.

A
  • Occurs in 30-40% diabetics
  • Typically begins with microalbuminuria
  • Progresses to proteinuria and, eventually, nephrotic syndrome
43
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 nodules
  • Stage 3: nodular lesions/Kimmelstein-Wilson nodules
  • Stage 4: advanced glomerulosclerosis
44
Q

What is amyloidosis?

A

Deposition of extracellular proteinaceous material exhibiting beta-pleated sheet structure

45
Q

What are the two types of amyloidosis?

A
  • AA - derived from serum amyloid associated protein (SAA), an acute phase protein, and associated with chronic inflammatory disease
  • AL - derived from immunoglobulin light chains usually as a result of multiple myeloma (80%)
46
Q

Describe the histological appearance of amyloidosis

A

Apple green birefringence with Congo red stain

47
Q

Name two causes of isolated / asymptomatic microscopic haematuria.

A
  • Thin basement membrane disease
  • IgA nephropathy
48
Q

How can the cause of asymptomatic proteinuria be confirmed?

A

Renal biopsy for histology, IHC, and electron microscopy (could be caused by several abnormalities)

49
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
50
Q

What is Alport syndrome?
What is its inheritance pattern?

A
  • X-linked dominant condition 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
51
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
  • Presents 1-2 days after an URTI with frank haematuria (earlier than acute post-infectious GN)
  • Immunofluorescence shows granular deposition of IgA and C3 in mesangium

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

52
Q

What is acute post-infectious (post-streptococcal) GN?

A
  • Occurs 1-3 weeks after streptococcal throat infection or impetigo (usually Lancefield Group A α-haemolytic strep = Strep. pyogenes)
  • Glomerular damage thought to be due to immune complex deposition
53
Q

What will a biopsy show in post-infectious GN?

A
  • Light microscope: ↑cellularity of glomeruli
  • Fluorescence Microscope: granular deposits of IgG and C3 in GBM
  • Electron Microscope: Subendothelial humps
54
Q

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

A
  • Diabetes mellitus (most common) - 27.5%
  • Glomerulonephritis - 14.1%
  • Polycystic kidney disease - 7.4%
  • Pyelonephritis - 6.5%
  • Hypertension - 6.8%
  • Renal vascular disease - 5.9%
55
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)
56
Q

What is the pathophysiology of hypertensive nephropathy?

A
  • Narrowing of arteries and arterioles leading to scarring and ischaemia of glomeruli
  • Hypertension in glomeruli leading to altered haemodynamic environment, stress and segmental scarring
57
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
58
Q

What system is used to classify lupus nephritis?

A

ISN/RPS classification

59
Q

Describe the histological appearance of lupus nephritis

A
  • Immune complex deposition in capillaries > ‘wire loop capillaries’ (thickened)
  • Deposition of immune complexes & complement in the GBM in a lumpy-bumpy granular fashion.
60
Q

What are the outcomes of lupus nephritis?

A

Highly variable

  • Acute renal failure
  • Nephrotic syndrome
  • Isolated urinary abnormality
  • CKD

Six stages:
• 1: Minimal mesangial disease, almost normal
• 2: Mesangial disease
• 3: Focal deposits
• 4: Diffuse deposits
• 5: Subepithelial membranous disease
• 6: Advanced sclerosis (>90%)

YEAR 5: Histopathology PM (COPY) (20 decks)

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