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Urinary > 8 > Flashcards

8 Flashcards

1
Q

In regards to the glomerulus, what does focal mean?

A

-involving less than 50% of the glomeruli on light microscopy

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2
Q

In regards to the glomeruli, what does diffuse mean?

A

-involving more than 50% of the glomeruli on light microscopy

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3
Q

In regards to glomeruli, what does segmental mean?

A

-involving part of the glomerular tuft

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4
Q

In regards to glomeruli, what does global mean?

A

-involving the entire glomerular tuft

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5
Q

In regards to glomeruli, what does membranous mean?

A

-thickening of the glomerular capillary wall

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6
Q

In regards to glomeruli, what does proliferative mean?

A

-increased number of cells in the glomerulus; these cells can be either proliferating glomerular cells or infiltrating circulating inflammatory cells

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7
Q

In regards to glomeruli, what does crescent mean?

A

-an accumulation of cells (mostly mononuclear) within the Bowman-s space; crescents often compress the capillary tuft and are associated with more sever disease

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8
Q

What is glomerulosclerosis?

A

-segmental or global capillary collapse, it is presumed that there is little to no filtration across sclerotic area

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9
Q

What is glomerulonephritis?

A

-any condition associated with inflammation in the glomerular tuft

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10
Q

What is the glomerulus?

A

-specialized structure adapted for filtration and regulating body homeostasis

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11
Q

What is the difference between nephrotic and nephritic syndrome?

A
  • Nephrotic: kidney loses significant amounts of protein so pt. Presents with frothy urine and generalized swelling, hypercholesterolaemia
  • Nephritic: acute renal failure, severe, hypertensive and haematuria
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12
Q

What is nephrotic syndrome?

A
  • clinical syndrome that can be initiated by a number of distinct aetiologies that lead to a shared pathogenic sequence
  • characterized by massive proteinuria and resultant hypoalbuminemia
  • patients display hyperlipidaemia

Nephrotic syndrome is a triad of:

  • Proteinuria > 350mg/mmol
  • Hypoalbuminaemia
  • Oedema
  • if pt. Doesn’t have all three then they dont have nephrotic syndrome
  • BP usually normal

Look at session 8-glomerular disease slide 8-11

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13
Q

What is the difference between primary and secondary injury to the glomerulus?

A
  • primary: will only affect the kidney

- secondary: will affect body AND kidney as well such as diabetes

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14
Q

What is nephrotic syndrome/proteinuria?

A
  • an insult to the glomerulus which results in loss of glomerular filtration barrier selectivity
  • selectivity is lost so it allows substantial filtration of plasma proteins which cannot undergo tubular resorption and are thus excreted in the urine, hence causing massive proteinuria

Likely site of injury
-podocytes, subepithelial damage, GBM

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15
Q

What are the common primary causes of nephrotic syndrome?

A
  • minimal change glomerulonephritis
  • focal segmental glomerulosclerosis (FSGS)
  • membranous glomerulonephritis
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16
Q

What are some common secondary causes of nephrotic syndrome?

A
  • diabetes mellitus

- connective tissue diseases

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17
Q

What is minimal change glomerulonephritis?

A
  • childhood/adolescence
  • incidence reduces with increasing age
  • heavy proteinuria or nephrotic syndrome
  • responds to steroids
  • may recur
  • usually no progression to renal failure
  • look at glomerular pathology slide 12
18
Q

What is minimal change in SGS spectrum?

A
  • little to no scarring
  • nephrotic
  • occurs in adults
  • less responsive to steroids
  • glomerulosclerosis
  • circulating factor damaging podocytes (transplants)
  • progressive to renal failure
19
Q

What is membranous glomerulonephritis?

A
  • commonest cause of primary nephrotic syndrome in adults
  • rule of thirds: 1/3 of patients will recover completely, 1/3 need ongoing treatment, 1/3 will get renal failure
  • Immune complex deposits (antibody/antigen)
  • may be secondary (associated with other disease ex. Lymphoma)
20
Q

What is the difference between haematuria and nephritic syndrome?

A

Haematuria

  • IgA nephropathy
  • thin glomerular BM disease/heridatary nephropathy (Alpert)

Nephritic syndrome

  • vasculitis
  • [Goodpasture Syndrome aka anti-GBM disease]
21
Q

What is IgA Nephropathy?

A
  • commonest glomerular nephropathy
  • any age
  • classically present with visible/invisible haematuria
  • relationship with mucosal infections
  • variable histological features and course
  • may have proteinuria
  • significant proportion progress to renal failure
  • no effective treatment
  • look at glomerular pathology slide 22-26
22
Q

List some hereditary nephropathies

A
  • thing GBM nephropathy
  • benign familiar nephropathy
  • isolated haematuria
  • thin GBM
  • benign course
  • alport
  • X linked
  • abnormal collagen IV
  • associated with deafness
  • abnormal appearing GBM
  • progresses to renal failure
  • can be quite a large grey area
  • see glomerular pathology slide 27-28
23
Q

What is vasculitis?

A
  • group of systemic disorders
  • no immune complex/antibody deposition
  • associated with Anti Neutropil Cytoplasmic Antibody (ANCA)
  • nephjritic presentation (RPGN)
  • treatable, IF caught early
  • urgent biopsy service
  • look at glomerular pathology slide 29-31
  • look at session 8-glomerua disease slide 15-16
24
Q

How does hypoalbuminaemia occur in nephrotic syndrome?

A
  • chronic excretion of plasma proteins reduces conc. Of albumin in plasma
  • decreased concentration resents in reduced plasma oncotic pressure which yields derangement of vascular Starling forces
  • result: increased filtration into ECF from systemic capillaries, often manifesting as generalized oedema
25
Q

Why is there chronic activation of RAAS in nephrotic syndrome?

A
  • because chronic loss of plasma fluids which reduces the systemic arterial pressure
  • activates the RAAS
  • but proteinuria means pressure is never achieved
26
Q

What is aetiology of Nephrotic syndrome?

A
  • initial change disease
  • membranous glomerulonephritis**
  • focal segmental glomerulosclerosis
  • diabetic nephropathy
  • renal amyloidosis
27
Q

What is nephritic syndrome?

A

-clinical syndrome that can be initiated by a number of distinct aetiologies that lead to a shared pathogenic sequence
-characterized by haematuria and pyruvate often with the presence of erythrocyte casts within the urine
-pt. Displays hypertension, azotemia, and oliguria
-caused by an inflammatory proces
-CLINICAL FEATURES: haematuria, reduction in GFR, hypertension
Look at session 8-glomerulus disease slide 8, 12-14

28
Q

Why is there reduced GFR in nephritic syndrome?

A
  • progressive damage to involved glomeruli
  • reduced GF reduces capacity for urine formation, causing oliguria
  • reduces clearance of metabolites, causing azotemia
  • also reduces capacity of kidneys to properly control long-term arterial pressure regulation, results in secondary hypertension
29
Q

What is aetiology of nephritic syndrome?

A
  • acute proliferative glomerulonephritis
  • IgA Nephropathy
  • Goodpasture Syndrome
  • Rapidly Progressive Glomerulonephritis
  • Alport Syndrome
  • Lupus nephritis
30
Q

How does diabetic nephropathy present?

A
  • earliest change: hyperfiltration and an increase in GFR
  • first sign: diabetes is microalbuminuria
  • histologically: there is thickening of the BM an mesangial expansion
  • at this point treatment intervention can halt the progress
  • over several years, overt proteinuria develops
  • CHARACtERISD by KIMMELSTIEL-WILSON NODULES, glomerulosclerosis and hyalinization of arterioles
31
Q

How can you manage diabetic nephropathy?

A

-good glycated is control
-control of glomerular hypertension
Look at session 8-glomerula disease slide 20

32
Q

What are the 4 structures in the glomerulus that can be damaged from glomerulonephritis?

A
  • capillary endothelium
  • glomerular BM
  • mesangial cells
  • podocytes
33
Q

What is the clinical presentation of GN?

A
  1. Asymptomatic haematuria and/or proteinuria (IgA, SLE, FSGS)
  2. Chronic glomerulonephritis (IgA, SLE, any treated GN)
  3. Acute glomerulonephritis (nephrotic syndrome, IgA, SLE, post-infectious, ANCA-vasculitis
  4. Rapidly progressive glomerulonephritis (often too quick for nephritic syndrome, ANCA-vasculitis, Goodpasture’s, post-infectious, SLE)
  5. Nephrotic syndrome (minimal change, FSGS, membranous, SLE)
34
Q

What is Anti-GBM disease (Goodpasture’s disease)?

A
  • a glomerulonephritis but not a vasculitis
  • caused by the productions of anti-bodies to a3 chain of type 4 collagen in glomerular basement membrane
  • can also affect a3 chain of type 4 collagen in alveolar BM but harder for anti-bodies to get here
  • pulmonary haemorrhage more likely with pre-existing damage to alveolar endothelium ex. Smokers, infection
  • results in a rapidly progressive glomerulonephritis
  • without treatment, mortality is >90%
35
Q

What is systemic lupus erythematosus?

A
  • type of vasculitis
  • can cause lots of different patterns of glomerulonephritis and not associated with one particular pattern
  • auto-immune systemic disease
  • can cause nephritic or nephrotic syndrome
  • prognosis depends on type of lesion, activity and amount of kidney involved
  • treatment also varies according to pattern of lupus nephritis
  • see session 8-glomerulus disease slide 18-19
36
Q

What is diabetic nephropathy?

A
  • commonest cause of end stage renal disease

- it is a GLOMERULOPATHY NOT A GLOMERULONEPHRITIS

37
Q

What are the pathological changes in diabetic nephropathy?

A
  1. Hyperfiltration
  2. Glomerular BM thickening
  3. Mesangial expansion (can have expansion without BM thickening and vice versa)
  4. Podocytes injury
  5. Glomerular sclerosis/arteriosclerosis
  • hyperfiltration and hypertension results in increase in GFR
  • look at session 8-glomerular disease slide 26-31
38
Q

What are the clinical signs and symptoms in diabetic nephropathy?

A
  1. Hyperfiltration and hypertrophy
    - increased GFR
  2. Latent stage
    - normal albuminuria
    - GBM thickening and mesangial expansion
  3. Microalbuminuria (aka moderately increased albuminuria)
    - variable mesangial expansion/sclerosis
    - increased GBM thickening
    - podocyte changes
    - GFR normal
  4. Overt proteinuria (aka severely increased albuminuria)
    - diffuse glomerular histopathological changes
    - systemic hypertension
    - falling GFR
  5. ESRD

Look at session 8-glomerular disease slide 33-38

39
Q

What are the risk factors for diabetic nephropathy?

A
  • genetic susceptibility
  • race
  • hypertension
  • hyperglycaemia
  • high level of hyperfiltration
  • increasing age
  • duration of diabetes
  • smoking
40
Q

What is the primary prevention of diabetic nephropathy?

A
  • tight blood glucose control
  • tight BP control
  • tight glycaemic control
  • look at session 8-glomerular disease slide 40-41
41
Q

How can we manage microalbuminuria and proteinuria?

A
  • inhibition of RAAS
  • tight BP control
  • statin therapy
  • CV risk management (exercise, diet, stop smoking)
  • moderate protein intake
  • tight blood glucose control (doesn’t affect progression once overt proteinuria develops)
42
Q

What is the RAAS blockade?

A
  • reduces glomerular hyperfiltration
  • efferent > afferent arterioles
  • anti-proteinuric effect more than BP reduction alone
  • reduces proteinuria and slows progression at stages 2-4 of diabetic nephropathy
  • hyperkalaemia limits use with advanced CKD

Urinary (11 decks)

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