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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
What are the main features of pauci-immune crescentic glomerulonephritis?
* Scanty glomerular immunoglobulin depositis * Usually associated with ANCA * Triggers neutrophil activation and glomerular necrosis
26
What is thrombotic microangiopathy?
* Damage to the endothelium in glomeruli, arteriols and arteries resulting in thrombosis * Red cells can be damaged by fibrin causing MAHA or HUS
27
List some causes of thrombotic microangiopathy.
* 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
28
What are the characteristic features of nephrotic syndrome?
* Proteinuria (\>3,5 g/day or \>300mg/mmol PCR) * Hypoalbuminaemia * Oedema * Hyperlipidaemia
29
List some causes of nephrotic syndrome.
* **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
30
What is minimal change disease?
* 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
31
Describe the histological appearance of focal segmental glomerulosclerosis.
Some glomeruli are partially scarred NOTE: this responds less well to immunosuppression
32
What is membranous glomerulonephritis?
* 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
Which antibodies are often found in primary membranous glomerulonephritis?
Antibodies against phospholipase A2 type M receptor (PLA2R)
34
Describe the typical progression of diabetic nephropathy.
Typically begins with microalbuminuria Progresses to proteinuria and, eventually, nephrotic syndrome
35
List and describe the stages of diabetic nephropathy.
* 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
What is amyloidosis?
Deposition of extracellular proteinaceous material exhibiting beta-pleated sheet structure
37
What are the two types of amyloidosis?
* 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
Name two causes of isolated microscopy haematuria.
* Thin basement membrane * IgA nephropathy
39
How can the cause of asymptomatic proteinuria be confirmed?
Renal biopsy (could be caused by several abnormalities)
40
What is thin basement membrane disease and what causes it?
* 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
What is Alport syndrome?
* 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
What is IgA nephropathy?
* 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
List some causes of chronic kidney disease and state which is most common.
* Diabetes mellitus * Glomerulonephritis * Polycystic kidney disease * Pyelonephritis * Hypertension * Renal vascular disease
44
What are some diseases associated with chronic kidney disease?
* Ischaemic heart disease * Calcium and phosphate derangement (due to resulting hyperparathyroidism, osteomalacia and osteoporosis)
45
What are consequences of hypertensive nephropathy?
* Shrunken kidneys with granular cortices * Nephrosclerosis on histology (arterial hyalinosis, arterial intimal thickening, ischaemic glomerular changes, segmental and global glomerulosclerosis)
46
What system is used to classify lupus nephritis?
ISI/RPS classification
47
What histological feature is suggestive of diabetic nephropathy?
Kimmelstein-Wilson nodules
48
What is another name for Alport's syndrome?
Hereditary nephritis
49
How do each of the primary causes of nephrotic syndrome respond to steroids?
MCD - well, 90% respond FSGS - 50% respond MN - poorly
50
What conditions are associated with MCD?
Asthma and eczema - may have an allergic component (e.g. sometimes triggered by recent allergic reaction)
51
What is the management of MCD?
1st line - steroids 2nd line - cyclosporin
52
What is the management of FSGS?
1st line - steroids 2nd line - calcineurinin inhibitors (e.g. tacrolimus)
53
Which ethnicity is diabetic nephropathy particularly associated with?
Asians
54
What are the symptoms of nephritic syndrome?
PHAROH Proteinuria - less significant than nephrotic syndrome Haematuria Azootemia - high creatinine and urea Red cell casts Oliguria Hypertension
55
What are the main causes of nephritic syndrome?
* Acute post-infectious (post-Strep) glomerulonephritis * IgA nephropathy (Berger's disease) * Rapidly progressive crescentic glomerulonephritis
56
What is typically the cause of post-infectious glomerulonephritis?
Lancefield Group A b-haemolytic Streptococcus (e.g. strep progenes) infection Such as impetigo or strep throat
57
What changes in blood tests would be seen in post-infectious glomerulonephritis?
Elevated ASOT (anti-streptolysin) titres Reduced C3
58
What changes on histology (light/fluoro/electron) would be seen in post-infectious glomerulonephritis?
Light - cellularity of glomeruli increased Fluorescence - IgG and C3 deposits in GBM Electron - subendothelial humps
59
What is the most common cause of glomerulonephritis worldwide?
IgA nephropathy
60
What is the classical presentation of IgA nephropathy?
* 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
What changes in blood tests would be seen in IgA nephropathy?
Raised IgA levels
62
What changes on histology would be seen in IgA nephropathy?
IgA and C3 deposits in mesangium
63
How can crescentic GN be differentiated from other causes of nephritic syndrome?
Oliguria and renal failure will often be more pronounced
64
What are some examples of Pauci-immune crescenteric GN?
* Wegner's granulomatosis (c-ANCA) * Microscopic polyangitis (p-ANCA)
65
What is acute interstitial nephritis?
Typically a hypersensitivity reaction, usually to a drug (NSAID, Abx, diuretics) that begins days after exposure to the drug
66
When is chronic interstitial nephritis seen?
Usually in elderly patients with chronic analgesic use (NSAIDs/paracetamol) with symptoms occurring late in disease
67
What is the triad of HUS?
* Thrombocytopenia * MAHA * Renal failure
68
What is the pentad of TTP?
* Thrombocytopenia * MAHA * Renal failure * Neurological symptoms - seizures, confusion * Fever
69
Why does TTP result in neurological symptoms?
Thrombi are not just confined to the kidneys (as in HUS) and instead can circulate, including the CNS
70
What blood test results would be expected in HUS/TTP?
* 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
What chromosome are the PKD mutations on respectively?
PKD1 = chromosome 16 PKD2 = chromosome 4
72
What are the clinical features of PKD?
MISHAPES Mass (abdominal) Infected cysts and Increased BP Stones Haematuria Aneursyms (berry) Polyuria and nocturia Extra-renal cysts Systolic murmur
73
Why might there be a systolic murmur in patients with PKD?
Mitral valve prolapse
74
Where can cysts occur outside of the kidneys in PKD?
Ovaries Liver Pancreas Seminal vesicles
75
What are some paraneoplastic syndromes associated with renal cell carcinoma?
Polycythaemia (increased EPO) Hypercalcaemia HTN Cushing's syndrome Amyloidosis

YEAR 5: Histopathology (20 decks)

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