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Year 5 Histopath > Renal > Flashcards

Renal Flashcards

1
Q

What are the 3 areas of the nephron upon which renal disease can be classified?

A

1) Glomerulus
2) Tubules & Interstitium
3) Blood vessels

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2
Q

Which renal diseases effect the glomerulus?

A

1) Nephrotic syndrome - breakdown of selectivity of glomerular filtration barrier
2) Nephritic syndrome

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3
Q

Which renal diseases effect the Tubules & interstitium?

A

1) Acute tubular necrosis

2) Tubulointerstitial nephritis

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4
Q

Which renal diseases effect the Blood vessels?

A

1) Thrombotic microangiopathies

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5
Q

What are the 2 thrombotic microangiopathies?

A

1) Haemolytic uraemic syndrome

2) Thrombotic thrombocytopenic purpura

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6
Q

What are the 3 types of tubulointerstitial nephritis?

A

1) Acute pyelonephritis
2) Chronic pyelonephritis & reflux nephropathy
3) Interstitial nephritis

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7
Q

Nephrotic syndrome is characterised by:

A

Proteinuria (>3g/24h) +
Hypoalbuminaemia +
Oedema
(+ Hyperlipidaemia)

Keywords: Frothy urine
Swelling - facially in kids and peripheral in adults

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8
Q

Primary causes of Nephrotic Syndrome are:

A

1) Minimal Change disease
2) Membranous Glomerular disease
3) Focal Segmental Glomerulosclerosis (FSGS)

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9
Q

Secondary causes of nephrotic syndrome are:

A

1) Diabetes

2) Amyloidosis

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10
Q

What is seen on light microscopy for primary causes of Nephrotic syndrome?

A

MC: No changes

MG: Diffuse glomerular basement membrane thickening

FSGS: Focal and segmental glomerular consolidation and scarring, Hyalinosis - abnormal accumulation of a clear (hyaline) substance in body tissue

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11
Q

What is seen on electron microscopy for primary causes of Nephrotic syndrome?

A

MC: Loss of podocyte foot processes

MG: Loss of podocyte foot processes
Subepithelial deposits ('Spikey')

FSGS: Loss of podocyte foot processes.

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12
Q

What is seen on immunofluorescence for primary causes of Nephrotic syndrome?

A

MC: No immune deposits

MG: Ig and complement in granular deposits along entire GBM

FSGS: Ig and complement in scarred areas

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13
Q

What is the prognosis of primary causes of Nephrotic syndrome?

A

MC:

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14
Q

How do primary causes of Nephrotic syndrome respond to steroids?

A

MC: 90% respond

MG: Poorly

FSGS: 50% respond

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15
Q

What is the epidemiology of primary causes of Nephrotic syndrome?

A

MC: Most common in children (75%) with 2nd peak in elderly

MG: Common in adults (~30%)

FSGS: Common in adults (~30%). Most common in Afro-Caribbean

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16
Q

Minimal Change disease

A

Common in children (2-3 yrs) and elderly
Loss of podocyte foot processes
No immune deposits
90% respond to steroids

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17
Q

Membranous Glomerular disease

A

Affecting adults between 30 - 50 years
Caucasian
Caused by immune complex formation in the glomerulus by binding of antibodies to antigens in the GBM. The antigens may be part of the basement membrane, or deposited from elsewhere by the systemic circulation.
The immune complex serves as an activator that triggers a response from the C5b - C9 complements, which form a membrane attack complex (MAC) on the glomerular epithelial cells. This, in turn, stimulates release of proteases and oxidants by the mesangial and epithelial cells, damaging the capillary walls and causing them to become “leaky”.
Diffuse GBM thickening on light microscopy
Loss of podocyte foot processes
Ig and complment in granular deposists along entire GBM
Can be 1o or 2o to SLE, infection, drugs and malignancyAffecting adults between 30 - 50 years
Caucasian

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18
Q

Focal Segmental Glomerulosclerosis (FSGS)

A

Leading cause of kidney failure in adults
Focal—only some of the glomeruli are involved (as opposed to diffuse), Segmental—only part of each glomerulus is involved (as opposed to global), Glomerulosclerosis—refers to scarring of the glomerulus
Most common in Afro-Carobbeans
Focal and segmental glomerular consolidation and scarring
Loss of podocyte foot processes on electron microscopy
1o but can be 2o to HIV nephropathy and obesity

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19
Q

Diabetes in secondary Nephrotic syndrome

A

Diffuse GBM thickening on histology

Mesangial matrix nodules - aka Kimmelstiel Wilson nodules

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20
Q

Amyloidosis in secondary Nephrotic syndrome

A

Apple green birefringence with congo red stain
Patient may also have:
Chronic inflammation - rheumatoid, chronic infections (TB) causing AA protein deposition
Immunoglobulin light chain deposition - AL protein deposition from multiple myeloma

Clinical clues: Macroglossia, heart failure, hepatomegaly

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21
Q

Define nephritic syndrome

A

A manifestation of glomerular inflammation (i.e. glomerulonephritis)

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22
Q

Nephritic syndrome is characterised by:

A

1) Haematuria (coca-cola urine)
2) Dysmporphic RBCs and red cell casts in urine

May also have:

3) Oliguria
4) Increased urea and creatinine
5) Hypertension
6) Proteinuria

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23
Q

Causes of nephritic syndrome

A

1) Acute postinfectious (post streptococcal) glomerulonephritis
2) IgA Nephropathy (berger disease)
3) Rapidly progressive (crescentic) GN
4) Hereditary nephritis (alports syndrome)
5) Thin basement membrane disease (benign familial haematuria)

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24
Q

What is the main difference between nephrotic and nephritic syndrome?

A

Nephrotic syndrome is characterized by only proteins moving into the urine. In contrast, Nephritic syndrome is characterized by having a thin glomerular basement membrane and small pores in the podocytes of the glomerulus, large enough to permit proteins (proteinuria) and red blood cells (hematuria) to pass into the urine. Both may involve hypoalbuminemia due to protein albumin moving from the blood to the urine.

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25
Q

How does acute postinfectious GN cause damage?

A

Glomerular damage is thought to be due to immune complex deposition
Occurs 1-3 weeks after streptococcal throat infection or impetigo (usually Group Aalpha-haemolytic strep = strep pyogenes)

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26
Q

How is acute postinfectious GN diagnosed?

A

Haematuria (red cell casts)
Proteinuria
Oedema
HTN

Bloods: antistreptococcal antibody (ASOT) titre is raised, C3 decreased

Biopsy:
Light microscope - increased cellularity of glomeruli
Flurescence microscope - granular deposits of IgG and C3 in GBM
Electron microscope - Subendothelial humps

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27
Q

Symptoms of IgA nephropathy (Berger disease)

A

Persistent or recurrent frank haematuria, or microscopic haematuria
Presents 1-2 days after a URTI with frank haematuria

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28
Q

What causes IgA nephropathy (berger disease)

A

Deposition of IgA immune complexes in the glomeruli
This is the most common GN worldwide
It can progress to ESRF

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29
Q

How is IgA nephropathy diagnosed?

A

Biopsy
Fluroescence microscopy shows granular deposition of IgA and complement in mesangium (the thin membrane supporting the capillary loops in renal glomeruli).

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30
Q

How does hereditary nephritis present?

A

Nephritic syndrome +
sensorineural deafness +
eye disorders (lens dislocation, cataracts)

Presents at 5-20 years with nephritic syndrome, progressing to ESRF

31
Q

How is hereditary nephritis caused?

A

X linked

Caused by a mutation in type IV collagen alpha 5 chain

32
Q

How is thin basement membrane disease caused?

A

Diffuse thinning of GBM caused by mutation in type IV collagen alpha 4 chain
Autosomal dominant

33
Q

What are the symptoms of thin basement membrane disease (benign familial haematuria)?

A

Very rarely a cause of nephritic syndrome - normally exclusively asymptomatic haematuria
Usually asymptomatic - incidentally diagnosed with microscopic haematuria
Renal function is usually normal

34
Q

3 causes of asymptomatic haematuria

A

1) Thin basement membrane disease (benign familial haematuria)
2) IgA nephropathy (berger disease)
3) Alports syndrome

35
Q

How does rapidly progressive (crescentic) GN present

A

Presents as nephritic syndrome but:

Oliguria + renal failure are more pronounced

36
Q

How is rapidly progressive (crescentic) GN classified?

A

Classification is based upon immunological findings:

Type 1: Anti-GBM antibody against COL4-A3 (collagen type IV)
Type 2: Immune complex
type 3: Pauci-immune/ANCA-associated

Regardless of causes, all are characterised by presence of crescents in the glomeruli.

37
Q

How is rapidly progressive (crescentic) GN caused?

A

Type 1: Goodpastures syndrome - HLA-DRB1 association
Type 2: SLE, IgA nephropathy, post infectious GN
Type 3: c-ANCA - Wegener’s granulomatosis
p-ANCA - microscopic polyangitis

38
Q

How does rapidly progressive (crescentic) GN present under fluorescence microscopy?

A

Type 1: Linear deposition of IgG in GBM

Type 2: Granular (lumpy bumpy) IgG immune complex deposition on GBM/mesangium

Type 3: Lack of/scanty significant immune complex deposition

39
Q

Additional organ involvements with crescentic GN

A

Type 1: Lungs - pulmonary haemorrhage

Type 3: Vasculitis - particularly presenting as skin rashes or pulmonary haemorrhage

40
Q

Define Acute Tubular Injury/Necrosis (ATI/ATN)

A

A severe form of acute renal failure that develops in people with severe illnesses (such as sepsis) or with very low blood pressure. Patients may need dialysis.
Most common cause of acute renal failure

41
Q

What is the mechanism of ATI/ATN?

A

Damage to tubular epithelial cells –> Blockage of tubules by casts –> reduced flow and haemodynamic changes –> acute renal failure

42
Q

What causes ATI/ATN?

A

Ischaemia - burns, septicaemia

Nephrotoxins - drugs (gentamicin, NSAIDs), radiographic contrast agents, myoglobin, heavy metals

43
Q

What is the histopathology of ATI/ATN?

A

Necrosis of short segments of tubules

44
Q

Define tubulointerstitial nephritis

A

A group of renal inflammatory disorders that involve the tubules and intersitium

45
Q

4 types of tubulointerstitial nephritis

A

1) Acute pyelonephritis
2) Chronic pyelonephritis & reflux nephropathy
3) Acute Interstitial nephritis
4) Chronic interstitial nephritis/Analgesic nephropathy

46
Q

Describe acute pyelonephritis

A

Bacterial infection of the kidney , usually as a result of ascending infection - E.coli

Presents with: fever
chills
sweats
flank pain
renal angle tendernesss
luekocytosis +/- frequency, dysuria and haematuria

Leukocytic casts are seen in urine

47
Q

Describe chronic pyelonephritis and reflux nephropathy

A

Chronic inflammation and scarring of the parenchyma caused by recurrent and persistent bacterial infection

Can be due to:
Chronic obstruction - posterior uretheral valves, renal calculi
Urine reflux (=reflux nephropathy)
48
Q

Describe Acute interstitial nephritis

A

A hypersensitivity reaction, usually to a drug e.g. Abx, NSAIDs, diuretics
Usually begins days after drug exposure

Presents with: fever
skin rash
haematuria
proteinuria
eosinophilia
49
Q

Describe Chronic interstitial nephritis/Analgesic nephropathy

A

Seen in the elderly with long-term analgesic consumption (NSAIDs/paracetamol)

Symptoms occur only in late disease: HTN, anaemia, proteinuria and haematuria

50
Q

What are 2 thrombotic Microangiopathies?

A

1) Haemolytic Uraemic Syndrome (HUS)

2) Thrombotic Thrombocytopaenic Purpura (TTP)

51
Q

What are thrombotic microangioplasties characterised by?

A 
Thrombosis
Triad of:
- Microangiopathic haemolytic anaemia (MAHA)
- Thrombocytopenia
- Renal failure
52
Q

What is the pathophysiology of thrombotic microangiopathies

A

widespread fibrin deposition in vessels -> formation of platelet-fibrin thrombi which damage passing platelets and RBC’s -> platelet and RBC destruction (i.e. thrombocytopenia and MAHA)

53
Q

Signs & symptoms of HUS and TTP:

A

decreased platelets -> bleeding (petechiae, haematemesis, melena)
MAHA -> pallor and jaundice

54
Q

Define thrombotic microangiopathy

A

thrombotic microangiopathies are microvascular occlusive disorders characterized by systemic or intrarenal aggregation of platelets, thrombocytopenia, and mechanical injury to erythrocytes. Itresults in thrombosis in capillaries and arterioles, due to an endothelial injury.

55
Q

DefineHemolytic uremic syndrome (HUS)

A

Hemolytic uremic syndrome (HUS) is a condition that results from the abnormal premature destruction of red blood cells. it ischaracterized by hemolytic anemia (anemia caused by destruction of red blood cells), acute kidney failure (uremia), and a low platelet count (thrombocytopenia).

56
Q

Define thrombotic thrombocytopenic purpura (TTP)

A

Thrombotic thrombocytopenic purpura (TTP) is a blood disorder that causes blood clots to form in small blood vessels. This leads to a low platelet count (thrombocytopenia).

57
Q

How to diagnose HUS and TTP

A 
Low Haemaglobin
Low platelets
Signs of haemolysis (Increased bilirubin, increased reticulocytes, increased LDH)
Fragmented RBC's on blood smear
Coomb's test negative (as not AIHA)
58
Q

HUS pathophysiology

A

Usually affects children
Usually associated with diarrhoea caused by E.coli (outbreaks caused by children visiting petting zoos)
can be non-diarrhoea associated due to abnormal proteins in complement pathway/endothelium - can be familial

Thrombi confined to kidneys
Usually involves renal failure

59
Q

TTP pathophysiology

A

Usually affects adults
Thrombi occur throughout circulation (esp in CNS)
Usually no renal failure
Neuro symptoms (headache, altered consciousness, seizures, coma)

60
Q

Define acute renal failure

A

the abrupt loss of kidney function, resulting in the retention of urea and creatinine

61
Q

Complications of acute renal failure are:

A 
Metabolic acidosis
Hyperkalaemia
Fluid overload
HTN
low calcium
Uraemia
62
Q

3 ways to characterise acute renal failure:

A

1) Pre-renal: Most common. Caused by renal hypo-perfusion e.g. hypovolaemia, sepsis, burns, acute pancreatitis and renal artery stenosis
2) Renal: Acute tubular necrosis is the most commenest cause but can also include acute glomerulonephritis and thrombotic microangiopathy
3) Post-renal: obstruction to urine flow as a result of stones, tumours (primary & secondary), prostatic hypertrophy and retroperitoneal fibrosis.

63
Q

Define chronic renal failure

A

Progressive, irreversible loss of renal function characterised by prolonged symptoms and signs of uraemia (fatigue, itching, anorexia and if severe eventually confusion)

64
Q

Signs & symptoms of uraemia in CKF

A

Fatigue
Itching
Anorexia
Confusion - if severe

65
Q

Causes of CRF

A 
Diabetes (19.5%)
Glomerulonephritis (15.3%)
HTN & Vascular disease (15%)
Reflux nephropathy (chronic pyelonephritis) (9.5%)
Polycystic kidney disease (9.4%)
66
Q

Staging classification of CRF

A

5 stages depending on GFR:

Stage 1: (>90) Kidney damage with normal renal function (often proteinurea)
Stage 2: (60-89) Mildly imparied
Stage 3: (30-59) Moderaterly impaired
Stage 4: (15-29) Severly impaired
Stage 5: (
67
Q

Defineadult polycystic kidney disease (APCKD)

A

a multisystemic and progressive disorder characterized by cyst formation and enlargement in the kidney and other organs (eg, liver, pancreas, spleen). It is autosomal dominant

68
Q

What mutations are present in APCKD?

A

There is autosomal dominant inheritence.
85% due to mutations in PKD1 on chromosome 16 (encoding polycystin-1)
15% in PKD2 on chromosome 4 (encoding polycystin-2)

69
Q

Clinical features of APCKD

A

Haematuria
Flank pain
UTI

Clinical features are usually due to cyst complications such as cyst rupture, cyst infection and cyst haemorrhage

70
Q

Pathogical features of APCKD

A

Large multicystic kidneys with destroyed renal parenchyma
Liver cysts (in PKD1)
Berry aneurysms

71
Q

Define Lupus Nephritis

A

Lupus nephritis is inflammation of the kidney that is caused by systemic lupus erythematous (SLE). Also called lupus, SLE is an autoimmune disease. With lupus, the body’s immune system targets its own body tissues. Lupus nephritis happens when lupus involves the kidneys.It is a type of glomerulonephritis in which the glomeruli become inflamed.

72
Q

Clinical presentation of lupus nephritis

A

Depending on site and intrsnity of immune complex deposition, presentation may be:

Isolated urinary abnormalities
Acute renal failure
Nephrotic syndrome
Progeressive chronic renal failure

73
Q

Classification of lupus nephritis

A

Class I: minimal mesangial lupus nephritis - immune complexes but no structural alteration

Class II: mesangial proliferative lupus nephritis - immune complexes and mild/moder increase in mesangial matrix and cellularity

Class III: focal lupus nephritis - active swelling and proliferation in less than half the glomeruli

Class IV: Diffuse lupus nephritis - involvement of more than half the glomeruli

Class V: membranous lupus nephritis - subepitherlial immune complex deposition

Class VI: advanced sclerosising - complete sclerosis of >90% of the glomeruli.

Year 5 Histopath (17 decks)

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